Hyperbaric oxygen therapy

evidence_span

{"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"}

experimental_model

Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement

exposure

100% oxygen at 2.5 ATA for three 20-minute periods

limitations

A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

One exposure leaves the cells better able to survive the next oxidative hit.

primary_references

[hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

tissue_or_cell_type

Circulating lymphocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 296–307

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement · source_derived_draft · unverified_draft

### hbot-adaptive-protection Blood taken 24 hours after treatment was significantly protected against DNA damage induced by hydrogen peroxide in vitro, while protection against gamma-irradiation was not significant. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: One exposure leaves the cells better able to survive the next oxidative hit. organism: Human tissue_or_cell_type: Circulating lymphocytes experimental_model: Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement limitations: A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron. exposure: 100% oxygen at 2.5 ATA for three 20-minute periods evidence_span: {"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"} [hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

evidence_span

{"source_cache": "artifacts/hbot-research/8941460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e", "start_char": 0, "end_char": 1910, "text_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e"}

experimental_model

Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer

exposure

Systemic hyperbaric oxygen, mean 38.8 sessions, added to a full treatment protocol

limitations

A single-centre randomised study with amputation as the endpoint. Adjunctive to an aggressive protocol, so the effect is of the addition, not of hyperbaric oxygen alone.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Fewer people in the treated group lost a limb in this trial.

primary_references

[hbot-p8941460] Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. A randomized study. (1996). https://pubmed.ncbi.nlm.nih.gov/8941460/ DOI: 10.2337/diacare.19.12.1338

tissue_or_cell_type

Foot

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 114–125

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer · source_derived_draft · unverified_draft

### hbot-amputation-reduction Major amputation occurred in 3 of 35 treated subjects (8.6%) versus 11 of 33 untreated (33.3%), a relative risk of 0.26, with the protective role confirmed on multivariate analysis. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Fewer people in the treated group lost a limb in this trial. organism: Human tissue_or_cell_type: Foot experimental_model: Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer limitations: A single-centre randomised study with amputation as the endpoint. Adjunctive to an aggressive protocol, so the effect is of the addition, not of hyperbaric oxygen alone. exposure: Systemic hyperbaric oxygen, mean 38.8 sessions, added to a full treatment protocol evidence_span: {"source_cache": "artifacts/hbot-research/8941460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e", "start_char": 0, "end_char": 1910, "text_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e"} [hbot-p8941460] Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. A randomized study. (1996). https://pubmed.ncbi.nlm.nih.gov/8941460/ DOI: 10.2337/diacare.19.12.1338

evidence_span

{"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"}

experimental_model

Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies

exposure

Hyperbaric oxygen with standard wound care for 20 days

limitations

A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Five different growth signals rose together in the treated wound.

primary_references

[hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

tissue_or_cell_type

Diabetic foot ulcer tissue

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 829–840

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

### hbot-angiogenic-markers Treatment increased tissue levels of the angiogenesis markers EGF, VEGF, PDGF, FGF-2 and CXCL10, and Nrf2 correlated positively with EGF, VEGF and PDGF. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Five different growth signals rose together in the treated wound. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

evidence_span

{"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"}

experimental_model

Twelve patients sampled at the first and fifteenth hyperbaric session

exposure

Fifteen hyperbaric oxygen treatments without antioxidant supplementation

limitations

A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The cell’s own defence enzymes measured lower, not higher, after repeated sessions.

primary_references

[hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

tissue_or_cell_type

Plasma and erythrocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 257–268

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve patients sampled at the first and fifteenth hyperbaric session · source_derived_draft · unverified_draft

### hbot-antioxidant-catalase After fifteen sessions, erythrocyte catalase activity fell significantly compared with the first exposure. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The cell’s own defence enzymes measured lower, not higher, after repeated sessions. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Twelve patients sampled at the first and fifteenth hyperbaric session limitations: A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation. exposure: Fifteen hyperbaric oxygen treatments without antioxidant supplementation evidence_span: {"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"} [hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

evidence_span

{"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"}

experimental_model

Twelve patients sampled at the first and fifteenth hyperbaric session

exposure

Fifteen hyperbaric oxygen treatments without antioxidant supplementation

limitations

A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The cell’s own defence enzymes measured lower, not higher, after repeated sessions.

primary_references

[hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

tissue_or_cell_type

Plasma and erythrocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 244–255

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve patients sampled at the first and fifteenth hyperbaric session · source_derived_draft · unverified_draft

### hbot-antioxidant-sod After fifteen sessions, erythrocyte superoxide dismutase activity fell significantly compared with the first exposure. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The cell’s own defence enzymes measured lower, not higher, after repeated sessions. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Twelve patients sampled at the first and fifteenth hyperbaric session limitations: A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation. exposure: Fifteen hyperbaric oxygen treatments without antioxidant supplementation evidence_span: {"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"} [hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

evidence_span

{"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"}

experimental_model

Rats poisoned with carbon monoxide, with leukocyte function assays

exposure

3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control

limitations

The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

The white cells still arrive and still work, but they cannot lock on and stay.

primary_references

[hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

tissue_or_cell_type

Brain microvasculature and polymorphonuclear leukocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 751–762

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats poisoned with carbon monoxide, with leukocyte function assays · source_derived_draft · unverified_draft

### hbot-b2-integrin-inhibition Hyperbaric oxygen did not inhibit the initial interaction of leukocytes with brain microvasculature, but persistent adherence, which is due to beta-2 integrins, did not occur; in vitro the leukocytes showed absent beta-2 integrin function while surface expression, elastase release and superoxide production on stimulation remained normal. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The white cells still arrive and still work, but they cannot lock on and stay. organism: Rat tissue_or_cell_type: Brain microvasculature and polymorphonuclear leukocytes experimental_model: Rats poisoned with carbon monoxide, with leukocyte function assays limitations: The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail. exposure: 3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control evidence_span: {"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"} [hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

evidence_span

{"source_cache": "artifacts/hbot-research/15050074.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970", "start_char": 0, "end_char": 1615, "text_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970"}

experimental_model

Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography

exposure

2.5 ATA for 90 minutes daily, 18 sessions preoperatively, after 22.4 Gy irradiation

limitations

A pre-treatment protocol in irradiated bone. Osteoblastic activity was measured by fluoride uptake, an activity surrogate.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rabbit

plain_language

The new vessels came back in the pattern healthy bone shows.

primary_references

[hbot-p15050074] Osteoblastic activity and neoangiogenesis in distracted bone of irradiated rabbit mandible with or without hyperbaric oxygen treatment. (2004). https://pubmed.ncbi.nlm.nih.gov/15050074/ DOI: 10.1054/ijom.2003.0489

tissue_or_cell_type

Mandibular bone

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1024–1035

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography · source_derived_draft · unverified_draft

### hbot-bone-neovascularisation The angiogenic response was markedly increased by hyperbaric oxygen, with blood vessels more numerous in the central region than peripheral regions in irradiated animals given the treatment, a pattern absent in irradiated animals without it. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The new vessels came back in the pattern healthy bone shows. organism: Rabbit tissue_or_cell_type: Mandibular bone experimental_model: Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography limitations: A pre-treatment protocol in irradiated bone. Osteoblastic activity was measured by fluoride uptake, an activity surrogate. exposure: 2.5 ATA for 90 minutes daily, 18 sessions preoperatively, after 22.4 Gy irradiation evidence_span: {"source_cache": "artifacts/hbot-research/15050074.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970", "start_char": 0, "end_char": 1615, "text_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970"} [hbot-p15050074] Osteoblastic activity and neoangiogenesis in distracted bone of irradiated rabbit mandible with or without hyperbaric oxygen treatment. (2004). https://pubmed.ncbi.nlm.nih.gov/15050074/ DOI: 10.1054/ijom.2003.0489

evidence_span

{"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"}

experimental_model

Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays

exposure

Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase

limitations

Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

Breathing oxygen under pressure narrows brain vessels rather than flooding them.

primary_references

[hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 153–164

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays · source_derived_draft · unverified_draft

### hbot-cbf-reduction After 30 minutes at 5 ATA, regional cerebral blood flow fell by 23 to 37% in substantia nigra, caudate putamen, hippocampus and parietal cortex. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Breathing oxygen under pressure narrows brain vessels rather than flooding them. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow measurement in rats with nitric oxide metabolite and hydroxyl radical assays limitations: Five atmospheres is well above therapeutic pressure and was chosen to study oxygen toxicity. The superoxide dismutase rescue is the key mechanistic step. exposure: Oxygen at 5 atmospheres absolute for 30 minutes, with L-NAME, a nitric oxide donor, or intravascular superoxide dismutase evidence_span: {"source_cache": "artifacts/hbot-research/11139368.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3", "start_char": 0, "end_char": 1672, "text_sha256": "9823a7f177483257b812d7c8c8e8052c3f04d6a7aa052876369c7c64b55668f3"} [hbot-p11139368] Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide. (2000). https://pubmed.ncbi.nlm.nih.gov/11139368/ DOI: 10.1006/niox.2000.0313

evidence_span

{"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"}

experimental_model

Regional cerebral blood flow and electroencephalography in anaesthetised rats

exposure

Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801

limitations

A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

The vessel response flips during a long exposure, and the flip comes just before the seizure activity.

primary_references

[hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 192–203

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow and electroencephalography in anaesthetised rats · source_derived_draft · unverified_draft

### hbot-cbf-time-course Blood flow fell by 26 to 43% at 3 and 4 ATA, but at 5 ATA it fell over 30 minutes then gradually returned to pre-exposure levels, preceding the onset of electroencephalographic spiking. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The vessel response flips during a long exposure, and the flip comes just before the seizure activity. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow and electroencephalography in anaesthetised rats limitations: A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss. exposure: Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801 evidence_span: {"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"} [hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

evidence_span

{"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"}

experimental_model

Human volunteers, mice, and endothelial nitric oxide synthase knockout mice

exposure

2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments

limitations

The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human and mouse

plain_language

The therapy calls stem cells out of the marrow into the blood.

primary_references

[hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

tissue_or_cell_type

Bone marrow and peripheral blood

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 530–541

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

### hbot-cd34-mobilisation CD34-positive cells in human peripheral blood doubled after a single 2.0 ATA exposure and rose eightfold over 20 treatments, without a significant increase in the overall white cell count. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The therapy calls stem cells out of the marrow into the blood. organism: Human and mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

evidence_span

{"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"}

experimental_model

Human volunteers, mice, and endothelial nitric oxide synthase knockout mice

exposure

2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments

limitations

The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human and mouse

plain_language

The mobilised cells carry the receptors for the two signals that guide them to a wound.

primary_references

[hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

tissue_or_cell_type

Bone marrow and peripheral blood

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 543–554

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

### hbot-cfc-increase Colony-forming cells rose from 16 to 26 per 100,000 monocytes plated, entirely due to the CD34-positive subpopulation, and a high proportion of progeny cells expressed receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The mobilised cells carry the receptors for the two signals that guide them to a wound. organism: Human and mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

evidence_span

{"source_cache": "artifacts/hbot-research/12362006.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1d5366f5eb1704ebe411ee13fba05068a310070c87ae65c8c75df678655dcca", "start_char": 0, "end_char": 1966, "text_sha256": "f1d5366f5eb1704ebe411ee13fba05068a310070c87ae65c8c75df678655dcca"}

experimental_model

Double-blind randomised trial of 152 patients with symptomatic acute carbon monoxide poisoning

exposure

Three hyperbaric oxygen sessions within 24 hours versus normobaric oxygen plus sham sessions

limitations

A randomised double-blind trial stopped early at a planned interim analysis, which tends to overstate effect size. Cerebellar dysfunction was imbalanced at baseline and was adjusted for.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Fewer people had lasting thinking problems after the treatment.

primary_references

[hbot-p12362006] Hyperbaric oxygen for acute carbon monoxide poisoning. (2002). https://pubmed.ncbi.nlm.nih.gov/12362006/ DOI: 10.1056/nejmoa013121

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1063–1074

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomised trial of 152 patients with symptomatic acute carbon monoxide poisoning · source_derived_draft · unverified_draft

### hbot-co-cognitive-benefit Cognitive sequelae at six weeks occurred in 25.0% of the hyperbaric group versus 46.1% of the normobaric group, an adjusted odds ratio of 0.45, and the difference persisted at 12 months. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Fewer people had lasting thinking problems after the treatment. organism: Human tissue_or_cell_type: Brain experimental_model: Double-blind randomised trial of 152 patients with symptomatic acute carbon monoxide poisoning limitations: A randomised double-blind trial stopped early at a planned interim analysis, which tends to overstate effect size. Cerebellar dysfunction was imbalanced at baseline and was adjusted for. exposure: Three hyperbaric oxygen sessions within 24 hours versus normobaric oxygen plus sham sessions evidence_span: {"source_cache": "artifacts/hbot-research/12362006.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1d5366f5eb1704ebe411ee13fba05068a310070c87ae65c8c75df678655dcca", "start_char": 0, "end_char": 1966, "text_sha256": "f1d5366f5eb1704ebe411ee13fba05068a310070c87ae65c8c75df678655dcca"} [hbot-p12362006] Hyperbaric oxygen for acute carbon monoxide poisoning. (2002). https://pubmed.ncbi.nlm.nih.gov/12362006/ DOI: 10.1056/nejmoa013121

evidence_span

{"source_cache": "artifacts/hbot-research/23423696.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2129b8a0c7356a65fbcedf4032e381f7dc22548282f894b785504f067fa6ced4", "start_char": 0, "end_char": 1491, "text_sha256": "2129b8a0c7356a65fbcedf4032e381f7dc22548282f894b785504f067fa6ced4"}

experimental_model

Longitudinal observational cohort of 6259 people in a wound care network, propensity-score adjusted

exposure

Hyperbaric oxygen as delivered under Medicare eligibility criteria

limitations

A large observational cohort, not a randomised trial. Propensity scores and an instrumental variable were used, but treatment selection by severity cannot be fully excluded; the direction of the result is opposite to the randomised study recorded alongside it.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

In routine care, the treated group did worse, not better.

primary_references

[hbot-p23423696] Lack of effectiveness of hyperbaric oxygen therapy for the treatment of diabetic foot ulcer and the prevention of amputation: a cohort study. (2013). https://pubmed.ncbi.nlm.nih.gov/23423696/ DOI: 10.2337/dc12-2160

tissue_or_cell_type

Foot

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 127–138

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Longitudinal observational cohort of 6259 people in a wound care network, propensity-score adjusted · source_derived_draft · unverified_draft

### hbot-cohort-no-benefit In propensity-score-adjusted models, individuals receiving hyperbaric oxygen were less likely to have their foot ulcer heal (hazard ratio 0.68) and more likely to have an amputation (2.37), and additional analyses including an instrumental variable did not change the result. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: In routine care, the treated group did worse, not better. organism: Human tissue_or_cell_type: Foot experimental_model: Longitudinal observational cohort of 6259 people in a wound care network, propensity-score adjusted limitations: A large observational cohort, not a randomised trial. Propensity scores and an instrumental variable were used, but treatment selection by severity cannot be fully excluded; the direction of the result is opposite to the randomised study recorded alongside it. exposure: Hyperbaric oxygen as delivered under Medicare eligibility criteria evidence_span: {"source_cache": "artifacts/hbot-research/23423696.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2129b8a0c7356a65fbcedf4032e381f7dc22548282f894b785504f067fa6ced4", "start_char": 0, "end_char": 1491, "text_sha256": "2129b8a0c7356a65fbcedf4032e381f7dc22548282f894b785504f067fa6ced4"} [hbot-p23423696] Lack of effectiveness of hyperbaric oxygen therapy for the treatment of diabetic foot ulcer and the prevention of amputation: a cohort study. (2013). https://pubmed.ncbi.nlm.nih.gov/23423696/ DOI: 10.2337/dc12-2160

evidence_span

{"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"}

experimental_model

Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies

exposure

Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers

limitations

Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The cells released carry more of the low-oxygen sensing proteins and more thioredoxin inside them.

primary_references

[hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

tissue_or_cell_type

Peripheral blood, platelets and skin wound margins

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 582–593

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies · source_derived_draft · unverified_draft

### hbot-diabetic-stem-mobilisation Diabetic patients showed a more than twofold elevation in circulating stem cells after treatments, and the post-treatment CD34-positive population contained two- to threefold higher levels of hypoxia inducible factors 1, 2 and 3 and of thioredoxin-1. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The cells released carry more of the low-oxygen sensing proteins and more thioredoxin inside them. organism: Human tissue_or_cell_type: Peripheral blood, platelets and skin wound margins experimental_model: Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies limitations: Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue. exposure: Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers evidence_span: {"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"} [hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

evidence_span

{"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"}

experimental_model

Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells

exposure

Hyperbaric oxygen with high glucose in vitro

limitations

Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Mouse and human cells

plain_language

Endothelial cells organise into tubes and fibroblasts start moving and dividing.

primary_references

[hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246

tissue_or_cell_type

Skin wound, fibroblasts and endothelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 673–684

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells · source_derived_draft · unverified_draft

### hbot-endothelial-tube Hyperbaric oxygen stimulated proliferation, migration and tube formation in human umbilical vein endothelial cells, and proliferation, migration and reactive oxygen species production in human skin fibroblasts. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Endothelial cells organise into tubes and fibroblasts start moving and dividing. organism: Mouse and human cells tissue_or_cell_type: Skin wound, fibroblasts and endothelium experimental_model: Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells limitations: Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person. exposure: Hyperbaric oxygen with high glucose in vitro evidence_span: {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"} [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246

evidence_span

{"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"}

experimental_model

Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies

exposure

Hyperbaric oxygen with standard wound care for 20 days

limitations

A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The same nitric oxide enzyme appears again, this time in the wound, with the immune cells joining in.

primary_references

[hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

tissue_or_cell_type

Diabetic foot ulcer tissue

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 842–853

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

### hbot-enos-nitrite-wound Expression of endothelial nitric oxide synthase and nitrite concentrations were significantly increased in treated subjects, and treatment sensitised macrophages to release FGF-2 and EGF while increasing the neutrophil attractant CXCL-8 and thereby the release of CCL2. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The same nitric oxide enzyme appears again, this time in the wound, with the immune cells joining in. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

evidence_span

{"source_cache": "artifacts/hbot-research/16984424.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a", "start_char": 0, "end_char": 1236, "text_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a"}

experimental_model

Human fibroblasts from normal skin and from chronic diabetic foot ulcers

exposure

One hour of hyperbaric oxygen at 106 to 300 kPa, with a hydrostatic pressure control

limitations

A dose-response in culture with a pressure control. The authors note the effects may not be due to oxygen availability alone.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cells

plain_language

There is a best pressure, and going higher does not help more.

primary_references

[hbot-p16984424] Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. (1997). https://pubmed.ncbi.nlm.nih.gov/16984424/ DOI: 10.1046/j.1524-475x.1997.50206.x

tissue_or_cell_type

Dermal fibroblasts

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 803–814

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human fibroblasts from normal skin and from chronic diabetic foot ulcers · source_derived_draft · unverified_draft

### hbot-fibroblast-dose-response A one-hour exposure at oxygen pressures between 106 and 300 kPa increased proliferation of both normal and diabetic fibroblasts, with a dose-dependent peak at 250 kPa for normal and 200 kPa for diabetic cells, and the effects were not due to hydrostatic pressure per se. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: There is a best pressure, and going higher does not help more. organism: Human cells tissue_or_cell_type: Dermal fibroblasts experimental_model: Human fibroblasts from normal skin and from chronic diabetic foot ulcers limitations: A dose-response in culture with a pressure control. The authors note the effects may not be due to oxygen availability alone. exposure: One hour of hyperbaric oxygen at 106 to 300 kPa, with a hydrostatic pressure control evidence_span: {"source_cache": "artifacts/hbot-research/16984424.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a", "start_char": 0, "end_char": 1236, "text_sha256": "59b39998f7e669db88fb2c3e69315ddfd6a1c52c82ab06997527991ac456d65a"} [hbot-p16984424] Dose-dependent hyperbaric oxygen stimulation of human fibroblast proliferation. (1997). https://pubmed.ncbi.nlm.nih.gov/16984424/ DOI: 10.1046/j.1524-475x.1997.50206.x

evidence_span

{"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"}

experimental_model

Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement

exposure

100% oxygen at 2.5 ATA for three 20-minute periods

limitations

A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The first session damages DNA; later sessions do not.

primary_references

[hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

tissue_or_cell_type

Circulating lymphocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 283–294

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement · source_derived_draft · unverified_draft

### hbot-first-exposure-dna-damage A single treatment caused clear and reproducible DNA damage in lymphocytes, found only after the first exposure and not after further treatments of the same individuals. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The first session damages DNA; later sessions do not. organism: Human tissue_or_cell_type: Circulating lymphocytes experimental_model: Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement limitations: A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron. exposure: 100% oxygen at 2.5 ATA for three 20-minute periods evidence_span: {"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"} [hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

evidence_span

{"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"}

experimental_model

Twelve patients sampled at the first and fifteenth hyperbaric session

exposure

Fifteen hyperbaric oxygen treatments without antioxidant supplementation

limitations

A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The selenium-dependent enzyme and the vitamin pools held steady while two other enzymes fell.

primary_references

[hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

tissue_or_cell_type

Plasma and erythrocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 270–281

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve patients sampled at the first and fifteenth hyperbaric session · source_derived_draft · unverified_draft

### hbot-gpx-unchanged Glutathione peroxidase activity remained almost unchanged, and no relevant differences were detected in reduced glutathione, alpha-tocopherol or retinol plasma levels. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The selenium-dependent enzyme and the vitamin pools held steady while two other enzymes fell. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Twelve patients sampled at the first and fifteenth hyperbaric session limitations: A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation. exposure: Fifteen hyperbaric oxygen treatments without antioxidant supplementation evidence_span: {"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"} [hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

evidence_span

{"source_cache": "artifacts/hbot-research/16325878.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e0360f0f818602bdcf74234be1b33779b854e82daadfdd69e78ad24eaa5953f", "start_char": 0, "end_char": 1115, "text_sha256": "6e0360f0f818602bdcf74234be1b33779b854e82daadfdd69e78ad24eaa5953f"}

experimental_model

Rat model of carbon monoxide poisoning with myelin basic protein chemistry, immunology and maze testing

exposure

Hyperbaric oxygen given after carbon monoxide poisoning

limitations

An immunological mechanism in a rat model. The treatment prevented the functional deficit without eliminating all the chemical changes, which is the informative dissociation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

The protein was still chemically altered, yet the immune attack and the disability did not follow.

primary_references

[hbot-p16325878] Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. (2006). https://pubmed.ncbi.nlm.nih.gov/16325878/ DOI: 10.1016/j.taap.2005.10.006

tissue_or_cell_type

Brain and immune system

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1089–1100

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat model of carbon monoxide poisoning with myelin basic protein chemistry, immunology and maze testing · source_derived_draft · unverified_draft

### hbot-hbo-prevents-immune-deficit Treatment prevented the functional deficit without eliminating all the chemical alterations in myelin basic protein: the protein was recognised normally by a battery of antibodies but retained an abnormal charge pattern, lymphocytes did not become activated, microglial activation was not apparent, and functional deficits did not occur. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The protein was still chemically altered, yet the immune attack and the disability did not follow. organism: Rat tissue_or_cell_type: Brain and immune system experimental_model: Rat model of carbon monoxide poisoning with myelin basic protein chemistry, immunology and maze testing limitations: An immunological mechanism in a rat model. The treatment prevented the functional deficit without eliminating all the chemical changes, which is the informative dissociation. exposure: Hyperbaric oxygen given after carbon monoxide poisoning evidence_span: {"source_cache": "artifacts/hbot-research/16325878.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e0360f0f818602bdcf74234be1b33779b854e82daadfdd69e78ad24eaa5953f", "start_char": 0, "end_char": 1115, "text_sha256": "6e0360f0f818602bdcf74234be1b33779b854e82daadfdd69e78ad24eaa5953f"} [hbot-p16325878] Hyperbaric oxygen reduces delayed immune-mediated neuropathology in experimental carbon monoxide toxicity. (2006). https://pubmed.ncbi.nlm.nih.gov/16325878/ DOI: 10.1016/j.taap.2005.10.006

evidence_span

{"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"}

experimental_model

Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells

exposure

Hyperbaric oxygen with high glucose in vitro

limitations

Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Mouse and human cells

plain_language

The signal and its receptor go up on two different cell types at once, which is what lets them find each other.

primary_references

[hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246

tissue_or_cell_type

Skin wound, fibroblasts and endothelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 660–671

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells · source_derived_draft · unverified_draft

### hbot-hif-vegf-sdf-axis Treatment promoted expression of HIF-1alpha, NF-kappaB, VEGFA, SDF-1, VEGFR2 and CXCR4, with SDF-1 and VEGFA rising in human skin fibroblasts and CXCR4 and VEGFR2 rising in endothelial cells. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The signal and its receptor go up on two different cell types at once, which is what lets them find each other. organism: Mouse and human cells tissue_or_cell_type: Skin wound, fibroblasts and endothelium experimental_model: Diabetic foot mouse model with human skin fibroblasts and human umbilical vein endothelial cells limitations: Cell and mouse work with expression endpoints. Tube formation is an angiogenesis surrogate, not a vessel in a person. exposure: Hyperbaric oxygen with high glucose in vitro evidence_span: {"source_cache": "artifacts/hbot-research/32791151.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188", "start_char": 0, "end_char": 1662, "text_sha256": "106ed876131af9161051c4c178d88af4afd707a20e56a91447d35aa9ed290188"} [hbot-p32791151] Hyperbaric oxygen potentiates diabetic wound healing by promoting fibroblast cell proliferation and endothelial cell angiogenesis. (2020). https://pubmed.ncbi.nlm.nih.gov/32791151/ DOI: 10.1016/j.lfs.2020.118246

evidence_span

{"source_cache": "artifacts/hbot-research/25532619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac", "start_char": 0, "end_char": 1943, "text_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac"}

experimental_model

Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice

exposure

Hyperbaric oxygen in vitro and in vivo, with adenoviral stable HIF-1alpha delivery

limitations

The knockout arm carries the causal claim. The authors describe the stabilisation as non-canonical, so the route from oxygen to HIF stability here is not the classical hydroxylase route.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cells and mouse

plain_language

More oxygen, not less, switched on the machinery that normally reads low oxygen.

primary_references

[hbot-p25532619] Hyperbaric oxygen therapy activates hypoxia-inducible factor 1 (HIF-1), which contributes to improved wound healing in diabetic mice. (2015). https://pubmed.ncbi.nlm.nih.gov/25532619/ DOI: 10.1111/wrr.12253

tissue_or_cell_type

Dermal fibroblasts and diabetic wounds

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 621–632

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice · source_derived_draft · unverified_draft

### hbot-hif1-activation Hyperbaric oxygen activated HIF-1alpha at several levels, increasing both its stability, by a mechanism the authors call non-canonical, and its activity, shown by induction of target genes and by a hypoxia-responsive-element reporter assay. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: More oxygen, not less, switched on the machinery that normally reads low oxygen. organism: Human cells and mouse tissue_or_cell_type: Dermal fibroblasts and diabetic wounds experimental_model: Human dermal fibroblasts, SKRC7 cells, HIF-1alpha knockout mouse embryonic fibroblasts, and db/db mice limitations: The knockout arm carries the causal claim. The authors describe the stabilisation as non-canonical, so the route from oxygen to HIF stability here is not the classical hydroxylase route. exposure: Hyperbaric oxygen in vitro and in vivo, with adenoviral stable HIF-1alpha delivery evidence_span: {"source_cache": "artifacts/hbot-research/25532619.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac", "start_char": 0, "end_char": 1943, "text_sha256": "bb139ca47291f581e4d45523657f9f244734ce42a3e44c5e460671e58946a3ac"} [hbot-p25532619] Hyperbaric oxygen therapy activates hypoxia-inducible factor 1 (HIF-1), which contributes to improved wound healing in diabetic mice. (2015). https://pubmed.ncbi.nlm.nih.gov/25532619/ DOI: 10.1111/wrr.12253

evidence_span

{"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"}

experimental_model

Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement

exposure

100% oxygen at 2.5 ATA for three 20-minute periods

limitations

A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Only one defence protein went up, and it is the one that handles heme iron.

primary_references

[hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

tissue_or_cell_type

Circulating lymphocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 309–320

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement · source_derived_draft · unverified_draft

### hbot-ho1-induction Heme oxygenase-1 levels were increased in lymphocytes 24 hours after treatment, while superoxide dismutase, catalase and the DNA repair enzymes apurinic endonuclease and DNA polymerase beta were not enhanced in expression. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Only one defence protein went up, and it is the one that handles heme iron. organism: Human tissue_or_cell_type: Circulating lymphocytes experimental_model: Comet assay in lymphocytes of volunteers before and after hyperbaric oxygen, with enzyme expression measurement limitations: A human exposure study with a within-subject design. The iron-sequestration explanation is the authors’ inference from the pattern of protection, not a direct measurement of free iron. exposure: 100% oxygen at 2.5 ATA for three 20-minute periods evidence_span: {"source_cache": "artifacts/hbot-research/11023535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d", "start_char": 0, "end_char": 1576, "text_sha256": "19b770dff3d327e2dd6d49180686f9823624190ab5693c28b88adcfaf703f14d"} [hbot-p11023535] Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment. (2000). https://pubmed.ncbi.nlm.nih.gov/11023535/ DOI: 10.1093/carcin/21.10.1795

evidence_span

{"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"}

experimental_model

Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors

exposure

A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation

limitations

A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

One heat shock protein responded strongly and the others barely moved.

primary_references

[hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967

tissue_or_cell_type

Primary spinal neurons

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 348–359

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors · source_derived_draft · unverified_draft

### hbot-hsp32-induction Heat shock protein 32 expression increased significantly and peaked 12 hours after exposure, while heat shock proteins 27, 70 and 90 showed only slight and non-significant increases. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: One heat shock protein responded strongly and the others barely moved. organism: Rat tissue_or_cell_type: Primary spinal neurons experimental_model: Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors limitations: A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin. exposure: A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation evidence_span: {"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"} [hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967

evidence_span

{"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"}

experimental_model

Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors

exposure

A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation

limitations

A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

Neurons preconditioned this way survived a later injury better.

primary_references

[hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967

tissue_or_cell_type

Primary spinal neurons

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 361–372

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors · source_derived_draft · unverified_draft

### hbot-hsp32-protection Preconditioning significantly increased cell viability and decreased lactate dehydrogenase release in cultures treated with hydrogen peroxide or oxygen-glucose deprivation. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Neurons preconditioned this way survived a later injury better. organism: Rat tissue_or_cell_type: Primary spinal neurons experimental_model: Primary rat spinal neurons after hyperbaric oxygen preconditioning with heat shock protein inhibitors limitations: A preconditioning experiment in cultured neurons. Heat shock protein 32 is heme oxygenase-1 under another name, which is why the inhibitor used is a porphyrin. exposure: A single hyperbaric oxygen exposure before hydrogen peroxide or oxygen-glucose deprivation evidence_span: {"source_cache": "artifacts/hbot-research/24465817.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f", "start_char": 0, "end_char": 1501, "text_sha256": "e79c9e686d7b5cab274a5bf6e25c188c42e44646fef7f478c53a12831de8e70f"} [hbot-p24465817] Hyperbaric oxygen preconditioning induces tolerance against oxidative injury and oxygen-glucose deprivation by up-regulating heat shock protein 32 in rat spinal neurons. (2014). https://pubmed.ncbi.nlm.nih.gov/24465817/ DOI: 10.1371/journal.pone.0085967

evidence_span

{"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"}

experimental_model

Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model

exposure

Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME

limitations

An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human and bovine cells

plain_language

The treatment switched off the docking molecule that inflamed vessels put out.

primary_references

[hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

tissue_or_cell_type

Vascular endothelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 712–723

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model · source_derived_draft · unverified_draft

### hbot-icam1-downregulation Induction of ICAM-1 required simultaneous hypoxia and hypoglycaemia, and hyperbaric oxygen reduced its expression to control levels. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The treatment switched off the docking molecule that inflamed vessels put out. organism: Human and bovine cells tissue_or_cell_type: Vascular endothelium experimental_model: Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model limitations: An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route. exposure: Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME evidence_span: {"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"} [hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

evidence_span

{"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"}

experimental_model

Human volunteers, mice, and endothelial nitric oxide synthase knockout mice

exposure

2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments

limitations

The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Mouse

plain_language

Nitric oxide rises inside the marrow itself, which is where the cells are released.

primary_references

[hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

tissue_or_cell_type

Bone marrow and peripheral blood

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 556–567

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human volunteers, mice, and endothelial nitric oxide synthase knockout mice · source_derived_draft · unverified_draft

### hbot-marrow-no-rise Bone marrow nitric oxide concentration increased by 1,008 nM in association with exposure, and circulating stem cell factor rose by 50% in mice with a 3.4-fold rise in cells expressing stem cell antigen-1 and CD34. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Nitric oxide rises inside the marrow itself, which is where the cells are released. organism: Mouse tissue_or_cell_type: Bone marrow and peripheral blood experimental_model: Human volunteers, mice, and endothelial nitric oxide synthase knockout mice limitations: The knockout and inhibitor arms carry the causal claim. Progenitor phenotype is defined by surface markers and colony formation, not by a demonstrated contribution to a healed vessel. exposure: 2.0 atmospheres absolute oxygen for 2 hours, single and over 20 treatments evidence_span: {"source_cache": "artifacts/hbot-research/16299259.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730", "start_char": 0, "end_char": 1502, "text_sha256": "76c0554557a30ac9a32f25b74b27edb5f8f8a57ee0c0660dfe5619b78732c730"} [hbot-p16299259] Stem cell mobilization by hyperbaric oxygen. (2006). https://pubmed.ncbi.nlm.nih.gov/16299259/ DOI: 10.1152/ajpheart.00888.2005

evidence_span

{"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"}

experimental_model

Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR

exposure

99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days

limitations

Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cells

plain_language

The damage landed on the mitochondria, and the cell could not make up the energy by fermenting.

primary_references

[hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

tissue_or_cell_type

Lens epithelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 413–424

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR · source_derived_draft · unverified_draft

### hbot-mito-damage-and-atp Cell death appeared to be caused by loss of ATP, with a 31% decrease immediately after exposure despite a 46% increase in lactate production, and damage occurred primarily in the mitochondria rather than the cytoplasm. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The damage landed on the mitochondria, and the cell could not make up the energy by fermenting. organism: Human cells tissue_or_cell_type: Lens epithelium experimental_model: Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR limitations: Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant. exposure: 99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days evidence_span: {"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"} [hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

evidence_span

{"source_cache": "artifacts/hbot-research/23770209.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a", "start_char": 0, "end_char": 1709, "text_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a"}

experimental_model

Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen

exposure

97.9% oxygen at 2.4 ATA for 90 minutes, with hyperbaric normoxia as a pressure control

limitations

A cell-line model of the neutrophil with a pressure control. The authors report that both hyperoxia and pressure contributed, without a consistent pattern.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cell line

plain_language

The same treatment also makes those cells die off on schedule, which is how inflammation ends.

primary_references

[hbot-p23770209] Effects of hyperbaric oxygen treatment on antimicrobial function and apoptosis of differentiated HL-60 (neutrophil-like) cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23770209/ DOI: 10.1016/j.lfs.2013.06.003

tissue_or_cell_type

Neutrophil-like cells

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1050–1061

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen · source_derived_draft · unverified_draft

### hbot-neutrophil-apoptosis-increase Pre-treatment had a pro-apoptotic effect, increasing caspase 3/7 activity and producing morphological changes associated with apoptosis, which the authors suggest may offset the potential detrimental effect of enhanced antimicrobial activity. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The same treatment also makes those cells die off on schedule, which is how inflammation ends. organism: Human cell line tissue_or_cell_type: Neutrophil-like cells experimental_model: Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen limitations: A cell-line model of the neutrophil with a pressure control. The authors report that both hyperoxia and pressure contributed, without a consistent pattern. exposure: 97.9% oxygen at 2.4 ATA for 90 minutes, with hyperbaric normoxia as a pressure control evidence_span: {"source_cache": "artifacts/hbot-research/23770209.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a", "start_char": 0, "end_char": 1709, "text_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a"} [hbot-p23770209] Effects of hyperbaric oxygen treatment on antimicrobial function and apoptosis of differentiated HL-60 (neutrophil-like) cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23770209/ DOI: 10.1016/j.lfs.2013.06.003

evidence_span

{"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"}

experimental_model

Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor

exposure

2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days

limitations

Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

Within a day the growth signals rise; within a week there are new vessels and repaired muscle.

primary_references

[hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

tissue_or_cell_type

Skeletal muscle

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 686–697

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor · source_derived_draft · unverified_draft

### hbot-no-vegf-bfgf Treatment significantly increased nitrate, VEGF and basic fibroblast growth factor levels and stabilised HIF-1alpha within one day, promoting blood vessel formation at 3 to 7 days and muscle healing at 5 to 7 days after contusion. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Within a day the growth signals rise; within a week there are new vessels and repaired muscle. organism: Rat tissue_or_cell_type: Skeletal muscle experimental_model: Contused rat skeletal muscle with a reactive oxygen species scavenger and a nitric oxide synthase inhibitor limitations: Both inhibitors were given before treatment, which is what makes the requirement claim interpretable. The exposure is a therapy-like protocol, unlike the extreme-pressure studies recorded elsewhere here. exposure: 2.5 ATA 100% oxygen for 120 minutes daily for 5 consecutive days evidence_span: {"source_cache": "artifacts/hbot-research/32066777.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d", "start_char": 0, "end_char": 1357, "text_sha256": "f8915aa50d5b22722e66d20eb0542c6bb03b76a3182d37215a53bc9238ac697d"} [hbot-p32066777] VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration. (2020). https://pubmed.ncbi.nlm.nih.gov/32066777/ DOI: 10.1038/s41598-020-59615-x

evidence_span

{"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"}

experimental_model

Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies

exposure

Hyperbaric oxygen with standard wound care for 20 days

limitations

A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The master switch for antioxidant defence is measurably higher in the treated wound.

primary_references

[hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

tissue_or_cell_type

Diabetic foot ulcer tissue

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 816–827

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies · source_derived_draft · unverified_draft

### hbot-nrf2-induction Tissue levels of Nrf2 and its downstream targets were significantly increased in patients receiving hyperbaric oxygen compared with standard therapy alone. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The master switch for antioxidant defence is measurably higher in the treated wound. organism: Human tissue_or_cell_type: Diabetic foot ulcer tissue experimental_model: Randomised comparison of 32 patients receiving standard wound care with or without hyperbaric oxygen, with ulcer tissue biopsies limitations: A small randomised human study with tissue-level molecular endpoints. Correlations between Nrf2 and growth factors are associations within treated tissue. exposure: Hyperbaric oxygen with standard wound care for 20 days evidence_span: {"source_cache": "artifacts/hbot-research/31035003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc", "start_char": 0, "end_char": 1966, "text_sha256": "e0b19a857412f1a255ecc82052eb403389bcf5596a562828c04558e1d4354efc"} [hbot-p31035003] Tissue-specific role of Nrf2 in the treatment of diabetic foot ulcers during hyperbaric oxygen therapy. (2019). https://pubmed.ncbi.nlm.nih.gov/31035003/ DOI: 10.1016/j.freeradbiomed.2019.04.031

evidence_span

{"source_cache": "artifacts/hbot-research/15050074.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970", "start_char": 0, "end_char": 1615, "text_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970"}

experimental_model

Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography

exposure

2.5 ATA for 90 minutes daily, 18 sessions preoperatively, after 22.4 Gy irradiation

limitations

A pre-treatment protocol in irradiated bone. Osteoblastic activity was measured by fluoride uptake, an activity surrogate.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rabbit

plain_language

Irradiated bone rebuilt more like healthy bone, without fully catching up.

primary_references

[hbot-p15050074] Osteoblastic activity and neoangiogenesis in distracted bone of irradiated rabbit mandible with or without hyperbaric oxygen treatment. (2004). https://pubmed.ncbi.nlm.nih.gov/15050074/ DOI: 10.1054/ijom.2003.0489

tissue_or_cell_type

Mandibular bone

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1011–1022

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography · source_derived_draft · unverified_draft

### hbot-osteoblast-activity Hyperbaric oxygen increased osteoblastic activity in irradiated distracted bone and shifted the osteogenic pattern towards that of non-irradiated bone, though not to the level of non-irradiated bone. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Irradiated bone rebuilt more like healthy bone, without fully catching up. organism: Rabbit tissue_or_cell_type: Mandibular bone experimental_model: Irradiated and non-irradiated rabbit mandibular distraction osteogenesis with fluoride autoradiography limitations: A pre-treatment protocol in irradiated bone. Osteoblastic activity was measured by fluoride uptake, an activity surrogate. exposure: 2.5 ATA for 90 minutes daily, 18 sessions preoperatively, after 22.4 Gy irradiation evidence_span: {"source_cache": "artifacts/hbot-research/15050074.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970", "start_char": 0, "end_char": 1615, "text_sha256": "1fe4a8f81ae5308f452c7a4551e9de0f0426daf32cbcd153149ec6e6a7a61970"} [hbot-p15050074] Osteoblastic activity and neoangiogenesis in distracted bone of irradiated rabbit mandible with or without hyperbaric oxygen treatment. (2004). https://pubmed.ncbi.nlm.nih.gov/15050074/ DOI: 10.1054/ijom.2003.0489

evidence_span

{"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"}

experimental_model

Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies

exposure

Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers

limitations

Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The enzyme that releases the cells stays switched on well after the session ends.

primary_references

[hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

tissue_or_cell_type

Peripheral blood, platelets and skin wound margins

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 608–619

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies · source_derived_draft · unverified_draft

### hbot-platelet-nos Nitric oxide synthase activity was acutely increased in patients’ platelets after treatment and remained elevated for at least 20 hours. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The enzyme that releases the cells stays switched on well after the session ends. organism: Human tissue_or_cell_type: Peripheral blood, platelets and skin wound margins experimental_model: Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies limitations: Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue. exposure: Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers evidence_span: {"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"} [hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

evidence_span

{"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"}

experimental_model

Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model

exposure

Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME

limitations

An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human and bovine cells

plain_language

With the docking molecule gone, the white cells no longer stick.

primary_references

[hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

tissue_or_cell_type

Vascular endothelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 725–736

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model · source_derived_draft · unverified_draft

### hbot-pmn-adhesion-drop Neutrophil adhesion to endothelial cells increased 3.4-fold after hypoxia and hypoglycaemia and was reduced to control levels by hyperbaric oxygen. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: With the docking molecule gone, the white cells no longer stick. organism: Human and bovine cells tissue_or_cell_type: Vascular endothelium experimental_model: Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model limitations: An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route. exposure: Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME evidence_span: {"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"} [hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

evidence_span

{"source_cache": "artifacts/hbot-research/18342453.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e54a071083cc14d5dcb6461692588b064f94d560a91045313836b0dca18cfe85", "start_char": 0, "end_char": 1963, "text_sha256": "e54a071083cc14d5dcb6461692588b064f94d560a91045313836b0dca18cfe85"}

experimental_model

Randomised controlled double-blind crossover trial of 150 patients with refractory radiation proctitis

exposure

2.0 atmospheres absolute versus air at 1.1 atmospheres absolute, with crossover

limitations

A double-blind crossover trial with a sham arm and five-year follow-up. The crossover abolished the between-group difference, which is consistent with a real treatment effect.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Most treated people improved, and the sham group improved too once they crossed over.

primary_references

[hbot-p18342453] Hyperbaric oxygen treatment of chronic refractory radiation proctitis: a randomized and controlled double-blind crossover trial with long-term follow-up. (2008). https://pubmed.ncbi.nlm.nih.gov/18342453/ DOI: 10.1016/j.ijrobp.2007.12.048

tissue_or_cell_type

Rectal mucosa

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1102–1113

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised controlled double-blind crossover trial of 150 patients with refractory radiation proctitis · source_derived_draft · unverified_draft

### hbot-radiation-proctitis-improvement Mean SOMA-LENT score improvement was nearly twice as large in the treated group (5.00 versus 2.61), with more responders per clinical assessment (88.9% versus 62.5%) and an absolute risk reduction of 32%, and the differences were abolished after crossover. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Most treated people improved, and the sham group improved too once they crossed over. organism: Human tissue_or_cell_type: Rectal mucosa experimental_model: Randomised controlled double-blind crossover trial of 150 patients with refractory radiation proctitis limitations: A double-blind crossover trial with a sham arm and five-year follow-up. The crossover abolished the between-group difference, which is consistent with a real treatment effect. exposure: 2.0 atmospheres absolute versus air at 1.1 atmospheres absolute, with crossover evidence_span: {"source_cache": "artifacts/hbot-research/18342453.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e54a071083cc14d5dcb6461692588b064f94d560a91045313836b0dca18cfe85", "start_char": 0, "end_char": 1963, "text_sha256": "e54a071083cc14d5dcb6461692588b064f94d560a91045313836b0dca18cfe85"} [hbot-p18342453] Hyperbaric oxygen treatment of chronic refractory radiation proctitis: a randomized and controlled double-blind crossover trial with long-term follow-up. (2008). https://pubmed.ncbi.nlm.nih.gov/18342453/ DOI: 10.1016/j.ijrobp.2007.12.048

evidence_span

{"source_cache": "artifacts/hbot-research/23770209.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a", "start_char": 0, "end_char": 1709, "text_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a"}

experimental_model

Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen

exposure

97.9% oxygen at 2.4 ATA for 90 minutes, with hyperbaric normoxia as a pressure control

limitations

A cell-line model of the neutrophil with a pressure control. The authors report that both hyperoxia and pressure contributed, without a consistent pattern.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cell line

plain_language

The cells that kill bacteria did so more strongly after a session.

primary_references

[hbot-p23770209] Effects of hyperbaric oxygen treatment on antimicrobial function and apoptosis of differentiated HL-60 (neutrophil-like) cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23770209/ DOI: 10.1016/j.lfs.2013.06.003

tissue_or_cell_type

Neutrophil-like cells

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1037–1048

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen · source_derived_draft · unverified_draft

### hbot-respiratory-burst-increase A single 90-minute exposure increased the respiratory burst activity of neutrophil-like cells after exposure, and phagocytosis of Staphylococcus aureus was also increased. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The cells that kill bacteria did so more strongly after a session. organism: Human cell line tissue_or_cell_type: Neutrophil-like cells experimental_model: Differentiated HL-60 neutrophil-like cells across normoxia, hypoxia, hyperoxia, pressure alone and hyperbaric oxygen limitations: A cell-line model of the neutrophil with a pressure control. The authors report that both hyperoxia and pressure contributed, without a consistent pattern. exposure: 97.9% oxygen at 2.4 ATA for 90 minutes, with hyperbaric normoxia as a pressure control evidence_span: {"source_cache": "artifacts/hbot-research/23770209.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a", "start_char": 0, "end_char": 1709, "text_sha256": "1621131d902e359cb8c23a51c1d76596ddff036697818a1613e68b26095eed8a"} [hbot-p23770209] Effects of hyperbaric oxygen treatment on antimicrobial function and apoptosis of differentiated HL-60 (neutrophil-like) cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23770209/ DOI: 10.1016/j.lfs.2013.06.003

evidence_span

{"source_cache": "artifacts/hbot-research/21200283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380", "start_char": 0, "end_char": 1120, "text_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380"}

experimental_model

Narrative review of therapeutic mechanisms and clinical trial evidence

exposure

Hyperbaric oxygen as used clinically, typically 2.0 to 2.5 atmospheres absolute

limitations

A narrative review, not a primary experiment. It is recorded as the framing source the reader was given; every mechanism it names is also recorded here from its own primary paper.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human, with supporting animal work

plain_language

The evidence is strongest for stubborn diabetic wounds and radiation damage, and thinner elsewhere.

primary_references

[hbot-p21200283] Hyperbaric oxygen: its mechanisms and efficacy. (2011). https://pubmed.ncbi.nlm.nih.gov/21200283/ DOI: 10.1097/prs.0b013e3181fbe2bf

tissue_or_cell_type

Multiple tissues

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 75–86

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Narrative review of therapeutic mechanisms and clinical trial evidence · source_derived_draft · unverified_draft

### hbot-review-efficacy-scope The review reports that systematic reviews and randomised clinical trials support clinical use of hyperbaric oxygen for refractory diabetic wound healing and radiation injuries, while compromised flaps, grafts and ischaemia-reperfusion disorders are supported by animal studies and a small number of clinical trials. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The evidence is strongest for stubborn diabetic wounds and radiation damage, and thinner elsewhere. organism: Human, with supporting animal work tissue_or_cell_type: Multiple tissues experimental_model: Narrative review of therapeutic mechanisms and clinical trial evidence limitations: A narrative review, not a primary experiment. It is recorded as the framing source the reader was given; every mechanism it names is also recorded here from its own primary paper. exposure: Hyperbaric oxygen as used clinically, typically 2.0 to 2.5 atmospheres absolute evidence_span: {"source_cache": "artifacts/hbot-research/21200283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380", "start_char": 0, "end_char": 1120, "text_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380"} [hbot-p21200283] Hyperbaric oxygen: its mechanisms and efficacy. (2011). https://pubmed.ncbi.nlm.nih.gov/21200283/ DOI: 10.1097/prs.0b013e3181fbe2bf

evidence_span

{"source_cache": "artifacts/hbot-research/21200283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380", "start_char": 0, "end_char": 1120, "text_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380"}

experimental_model

Narrative review of therapeutic mechanisms and clinical trial evidence

exposure

Hyperbaric oxygen as used clinically, typically 2.0 to 2.5 atmospheres absolute

limitations

A narrative review, not a primary experiment. It is recorded as the framing source the reader was given; every mechanism it names is also recorded here from its own primary paper.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human, with supporting animal work

plain_language

The therapy works by making the cell produce reactive molecules that carry signals, not simply by supplying more oxygen.

primary_references

[hbot-p21200283] Hyperbaric oxygen: its mechanisms and efficacy. (2011). https://pubmed.ncbi.nlm.nih.gov/21200283/ DOI: 10.1097/prs.0b013e3181fbe2bf

tissue_or_cell_type

Multiple tissues

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 62–73

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Narrative review of therapeutic mechanisms and clinical trial evidence · source_derived_draft · unverified_draft

### hbot-review-reactive-species-framing The review states that the principal mechanisms of hyperbaric oxygen are based on intracellular generation of reactive species of oxygen and nitrogen, which act through cell signal transduction cascades. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The therapy works by making the cell produce reactive molecules that carry signals, not simply by supplying more oxygen. organism: Human, with supporting animal work tissue_or_cell_type: Multiple tissues experimental_model: Narrative review of therapeutic mechanisms and clinical trial evidence limitations: A narrative review, not a primary experiment. It is recorded as the framing source the reader was given; every mechanism it names is also recorded here from its own primary paper. exposure: Hyperbaric oxygen as used clinically, typically 2.0 to 2.5 atmospheres absolute evidence_span: {"source_cache": "artifacts/hbot-research/21200283.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380", "start_char": 0, "end_char": 1120, "text_sha256": "541f2eb700a843e35093e589069b7839f1a3577c2de8cd1edb444698c1379380"} [hbot-p21200283] Hyperbaric oxygen: its mechanisms and efficacy. (2011). https://pubmed.ncbi.nlm.nih.gov/21200283/ DOI: 10.1097/prs.0b013e3181fbe2bf

evidence_span

{"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"}

experimental_model

Twelve patients sampled at the first and fifteenth hyperbaric session

exposure

Fifteen hyperbaric oxygen treatments without antioxidant supplementation

limitations

A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Repeated treatment leaves measurable marks of oxidation in the blood.

primary_references

[hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

tissue_or_cell_type

Plasma and erythrocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 231–242

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve patients sampled at the first and fifteenth hyperbaric session · source_derived_draft · unverified_draft

### hbot-rom-accumulation Repeated exposures led to significant accumulation of plasma reactive oxygen metabolites and malondialdehyde across fifteen sessions. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Repeated treatment leaves measurable marks of oxidation in the blood. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Twelve patients sampled at the first and fifteenth hyperbaric session limitations: A small human series without a control group. The fall in enzyme activity may reflect oxidative modification of the enzymes themselves, which the authors state was still under investigation. exposure: Fifteen hyperbaric oxygen treatments without antioxidant supplementation evidence_span: {"source_cache": "artifacts/hbot-research/15003734.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f", "start_char": 0, "end_char": 1432, "text_sha256": "5e4b6cef5c64b735c97ae362e7a90c76433e3f8fef2978d3b3b2a584016e506f"} [hbot-p15003734] Oxidative stress and antioxidant status in patients undergoing prolonged exposure to hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15003734/ DOI: 10.1016/j.clinbiochem.2003.12.001

evidence_span

{"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"}

experimental_model

Regional cerebral blood flow and electroencephalography in anaesthetised rats

exposure

Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801

limitations

A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

The seizure and the blood-flow change are separate events with separate causes.

primary_references

[hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

tissue_or_cell_type

Brain

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 218–229

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Regional cerebral blood flow and electroencephalography in anaesthetised rats · source_derived_draft · unverified_draft

### hbot-seizure-glutamate-independent-flow The NMDA receptor inhibitor MK-801 did not alter the cerebrovascular responses to oxygen at 5 ATA but prevented the electroencephalographic spikes. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The seizure and the blood-flow change are separate events with separate causes. organism: Rat tissue_or_cell_type: Brain experimental_model: Regional cerebral blood flow and electroencephalography in anaesthetised rats limitations: A time-course study at toxic pressures. It shows the nitric oxide effect reverses with exposure time, which a single time point would miss. exposure: Oxygen at 1, 3, 4 and 5 ATA with L-NAME, L-arginine, nitric oxide donors or MK-801 evidence_span: {"source_cache": "artifacts/hbot-research/10749833.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687", "start_char": 0, "end_char": 1283, "text_sha256": "1470d09e77b6d6f6af3131a6f7db2cca647dde3655662a1c83f9d5d375f1c687"} [hbot-p10749833] Nitric oxide and cerebral blood flow responses to hyperbaric oxygen. (2000). https://pubmed.ncbi.nlm.nih.gov/10749833/ DOI: 10.1152/jappl.2000.88.4.1381

evidence_span

{"source_cache": "artifacts/hbot-research/15559001.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5507526d06e294cc1dfe4ce0be912be957c850b3d7e8243c7fd947c5a10c2c82", "start_char": 0, "end_char": 1303, "text_sha256": "5507526d06e294cc1dfe4ce0be912be957c850b3d7e8243c7fd947c5a10c2c82"}

experimental_model

Retrospective review of 80,679 patient-treatments in two university hyperbaric departments

exposure

Routine hyperbaric oxygen protocols, including 2.4 ATA by mask with air breaks

limitations

A retrospective incidence count. It describes risk under appropriate exclusion criteria and treatment profiles, and does not estimate risk for an individual.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The feared brain side effect happened about twice in eighty thousand treatments.

primary_references

[hbot-p15559001] Seizure incidence in 80,000 patient treatments with hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15559001/

tissue_or_cell_type

Central nervous system

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 140–151

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective review of 80,679 patient-treatments in two university hyperbaric departments · source_derived_draft · unverified_draft

### hbot-seizure-incidence Two seizures were documented in 80,679 patient-treatments, an incidence of 2.4 per 100,000 patient-treatments, both in a multiplace chamber at 2.4 ATA with oxygen by mask. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The feared brain side effect happened about twice in eighty thousand treatments. organism: Human tissue_or_cell_type: Central nervous system experimental_model: Retrospective review of 80,679 patient-treatments in two university hyperbaric departments limitations: A retrospective incidence count. It describes risk under appropriate exclusion criteria and treatment profiles, and does not estimate risk for an individual. exposure: Routine hyperbaric oxygen protocols, including 2.4 ATA by mask with air breaks evidence_span: {"source_cache": "artifacts/hbot-research/15559001.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5507526d06e294cc1dfe4ce0be912be957c850b3d7e8243c7fd947c5a10c2c82", "start_char": 0, "end_char": 1303, "text_sha256": "5507526d06e294cc1dfe4ce0be912be957c850b3d7e8243c7fd947c5a10c2c82"} [hbot-p15559001] Seizure incidence in 80,000 patient treatments with hyperbaric oxygen. (2004). https://pubmed.ncbi.nlm.nih.gov/15559001/

evidence_span

{"source_cache": "artifacts/hbot-research/33206062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf", "start_char": 0, "end_char": 1622, "text_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf"}

experimental_model

Prospective trial of 35 healthy independently living adults aged 64 and over

exposure

Sixty daily hyperbaric oxygen exposures, sampled at baseline, 30 and 60 sessions and after the course

limitations

A single-arm prospective trial without a control group, in a normal ageing population. Telomere length and senescent-cell percentage are cell measurements, not health outcomes.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

Fewer worn-out immune cells were left in circulation.

primary_references

[hbot-p33206062] Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33206062/ DOI: 10.18632/aging.202188

tissue_or_cell_type

Peripheral blood mononuclear cells

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1128–1139

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective trial of 35 healthy independently living adults aged 64 and over · source_derived_draft · unverified_draft

### hbot-senescent-cell-clearance Senescent T helper cells fell by 37.30% and senescent T cytotoxic cells by 10.96% after the course. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Fewer worn-out immune cells were left in circulation. organism: Human tissue_or_cell_type: Peripheral blood mononuclear cells experimental_model: Prospective trial of 35 healthy independently living adults aged 64 and over limitations: A single-arm prospective trial without a control group, in a normal ageing population. Telomere length and senescent-cell percentage are cell measurements, not health outcomes. exposure: Sixty daily hyperbaric oxygen exposures, sampled at baseline, 30 and 60 sessions and after the course evidence_span: {"source_cache": "artifacts/hbot-research/33206062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf", "start_char": 0, "end_char": 1622, "text_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf"} [hbot-p33206062] Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33206062/ DOI: 10.18632/aging.202188

evidence_span

{"source_cache": "artifacts/hbot-research/8941460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e", "start_char": 0, "end_char": 1910, "text_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e"}

experimental_model

Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer

exposure

Systemic hyperbaric oxygen, mean 38.8 sessions, added to a full treatment protocol

limitations

A single-centre randomised study with amputation as the endpoint. Adjunctive to an aggressive protocol, so the effect is of the addition, not of hyperbaric oxygen alone.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

The treatment measurably raised the oxygen reaching the skin of the foot.

primary_references

[hbot-p8941460] Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. A randomized study. (1996). https://pubmed.ncbi.nlm.nih.gov/8941460/ DOI: 10.2337/diacare.19.12.1338

tissue_or_cell_type

Foot

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 101–112

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer · source_derived_draft · unverified_draft

### hbot-tcpo2-rise Transcutaneous oxygen tension measured on the dorsum of the foot rose significantly more in the treated group, by 14.0 mmHg versus 5.0 mmHg. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The treatment measurably raised the oxygen reaching the skin of the foot. organism: Human tissue_or_cell_type: Foot experimental_model: Randomised study of 70 people admitted with severe prevalently ischaemic diabetic foot ulcer limitations: A single-centre randomised study with amputation as the endpoint. Adjunctive to an aggressive protocol, so the effect is of the addition, not of hyperbaric oxygen alone. exposure: Systemic hyperbaric oxygen, mean 38.8 sessions, added to a full treatment protocol evidence_span: {"source_cache": "artifacts/hbot-research/8941460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e", "start_char": 0, "end_char": 1910, "text_sha256": "2f2904fa77e07a14257977ef8ca30fc46ee5ada35e65be2cc6512161bd0b440e"} [hbot-p8941460] Adjunctive systemic hyperbaric oxygen therapy in treatment of severe prevalently ischemic diabetic foot ulcer. A randomized study. (1996). https://pubmed.ncbi.nlm.nih.gov/8941460/ DOI: 10.2337/diacare.19.12.1338

evidence_span

{"source_cache": "artifacts/hbot-research/33206062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf", "start_char": 0, "end_char": 1622, "text_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf"}

experimental_model

Prospective trial of 35 healthy independently living adults aged 64 and over

exposure

Sixty daily hyperbaric oxygen exposures, sampled at baseline, 30 and 60 sessions and after the course

limitations

A single-arm prospective trial without a control group, in a normal ageing population. Telomere length and senescent-cell percentage are cell measurements, not health outcomes.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

A marker of cell ageing moved in the opposite direction to ageing.

primary_references

[hbot-p33206062] Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33206062/ DOI: 10.18632/aging.202188

tissue_or_cell_type

Peripheral blood mononuclear cells

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 1115–1126

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective trial of 35 healthy independently living adults aged 64 and over · source_derived_draft · unverified_draft

### hbot-telomere-lengthening Telomere length of T helper, T cytotoxic, natural killer and B cells increased by over 20% after 60 sessions, with B cells rising 37.63% after the course. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: A marker of cell ageing moved in the opposite direction to ageing. organism: Human tissue_or_cell_type: Peripheral blood mononuclear cells experimental_model: Prospective trial of 35 healthy independently living adults aged 64 and over limitations: A single-arm prospective trial without a control group, in a normal ageing population. Telomere length and senescent-cell percentage are cell measurements, not health outcomes. exposure: Sixty daily hyperbaric oxygen exposures, sampled at baseline, 30 and 60 sessions and after the course evidence_span: {"source_cache": "artifacts/hbot-research/33206062.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf", "start_char": 0, "end_char": 1622, "text_sha256": "3ac16eb39be25c350e6a42fff6ee8cbf22159514a750bc3c7bafcbf734f03ecf"} [hbot-p33206062] Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial. (2020). https://pubmed.ncbi.nlm.nih.gov/33206062/ DOI: 10.18632/aging.202188

evidence_span

{"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"}

experimental_model

Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR

exposure

99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days

limitations

Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cells

plain_language

Of all the defences measured, the selenium enzyme was the one that was knocked down.

primary_references

[hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

tissue_or_cell_type

Lens epithelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 387–398

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR · source_derived_draft · unverified_draft

### hbot-trxr-activity-loss Thioredoxin reductase activity fell by 51% after the 3-hour oxygen exposure, while cellular glutathione and the activities of several other antioxidant enzymes, including glyceraldehyde-3-phosphate dehydrogenase, showed no immediate effect. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Of all the defences measured, the selenium enzyme was the one that was knocked down. organism: Human cells tissue_or_cell_type: Lens epithelium experimental_model: Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR limitations: Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant. exposure: 99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days evidence_span: {"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"} [hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

evidence_span

{"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"}

experimental_model

Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR

exposure

99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days

limitations

Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human cells

plain_language

The cell rebuilt exactly three proteins: the heme enzyme, the manganese enzyme and the selenium enzyme.

primary_references

[hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

tissue_or_cell_type

Lens epithelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 426–437

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR · source_derived_draft · unverified_draft

### hbot-trxr-mrna-response Messenger RNA for heme oxygenase-1, manganese superoxide dismutase and cytoplasmic thioredoxin reductase 1 rose three- to six-fold nine hours after exposure, with heme oxygenase-1 rising a few hours before manganese superoxide dismutase, while catalase, copper-zinc superoxide dismutase, glutathione reductase, glutathione peroxidase and thioredoxin did not change. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The cell rebuilt exactly three proteins: the heme enzyme, the manganese enzyme and the selenium enzyme. organism: Human cells tissue_or_cell_type: Lens epithelium experimental_model: Cultured human lens epithelial cells exposed to extreme hyperbaric oxygen with enzyme assays and real-time PCR limitations: Fifty atmospheres is an extreme experimental exposure far above therapy, chosen to probe which defences matter. The selenoenzyme result is the informative part; the pressure is not clinically relevant. exposure: 99% oxygen at 50 atmospheres for 3 hours, then normal culture for up to 11 days evidence_span: {"source_cache": "artifacts/hbot-research/15642322.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995", "start_char": 0, "end_char": 2646, "text_sha256": "e3bc035a17e4e19dd92d4fadb1a79f8e3801619dac24fb91dcf985728afaf995"} [hbot-p15642322] Thioredoxin reductase may be essential for the normal growth of hyperbaric oxygen-treated human lens epithelial cells. (2004). https://pubmed.ncbi.nlm.nih.gov/15642322/ DOI: 10.1016/j.exer.2004.07.001

evidence_span

{"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"}

experimental_model

Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies

exposure

Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers

limitations

Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human

plain_language

More of these cells and proteins turn up at the wound itself, and a fresh wound starts from a better position than a chronic one.

primary_references

[hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

tissue_or_cell_type

Peripheral blood, platelets and skin wound margins

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 595–606

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies · source_derived_draft · unverified_draft

### hbot-wound-recruitment Expression of CD133, CD34, hypoxia inducible factor-1 and thioredoxin-1 in wound margins increased with treatment, and was higher in 2-day-old abdominal wounds than in refractory lower-extremity wounds. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: More of these cells and proteins turn up at the wound itself, and a fresh wound starts from a better position than a chronic one. organism: Human tissue_or_cell_type: Peripheral blood, platelets and skin wound margins experimental_model: Diabetic patients undergoing hyperbaric oxygen for refractory neuropathic ulcers, with wound margin biopsies limitations: Human observational measurements within a treatment course, without a randomised comparison. Protein content is measured in the mobilised cells, not in healed tissue. exposure: Clinical hyperbaric oxygen therapy courses for refractory lower-extremity ulcers evidence_span: {"source_cache": "artifacts/hbot-research/21362081.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b", "start_char": 0, "end_char": 1077, "text_sha256": "a830ae6900d884b73f4e5eac335263db6f9d981a0f95aa45ad3e266c44800e0b"} [hbot-p21362081] Vasculogenic stem cell mobilization and wound recruitment in diabetic patients: increased cell number and intracellular regulatory protein content associated with hyperbaric oxygen therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/21362081/ DOI: 10.1111/j.1524-475x.2010.00660.x

evidence_span

{"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"}

experimental_model

Rats poisoned with carbon monoxide, with leukocyte function assays

exposure

3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control

limitations

The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Rat

plain_language

Stopping the white cells sticking stops the enzyme switch that generates the damage.

primary_references

[hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

tissue_or_cell_type

Brain microvasculature and polymorphonuclear leukocytes

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 764–775

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats poisoned with carbon monoxide, with leukocyte function assays · source_derived_draft · unverified_draft

### hbot-xanthine-oxidase-prevention Exposure inhibited carbon monoxide-mediated brain lipid peroxidation by preventing the conversion of xanthine dehydrogenase to oxidase, a conversion known to be due to the action of leukocytes. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Stopping the white cells sticking stops the enzyme switch that generates the damage. organism: Rat tissue_or_cell_type: Brain microvasculature and polymorphonuclear leukocytes experimental_model: Rats poisoned with carbon monoxide, with leukocyte function assays limitations: The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail. exposure: 3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control evidence_span: {"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"} [hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

evidence_span

{"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"}

experimental_model

Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model

exposure

Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME

limitations

An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route.

nutrient_topic

Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

organism

Human and bovine cells

plain_language

The effect runs through the nitric oxide enzyme the vessel wall makes.

primary_references

[hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

tissue_or_cell_type

Vascular endothelium

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 738–749

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model · source_derived_draft · unverified_draft

### hbot-enos-mediates-icam Exposure induced endothelial nitric oxide synthase synthesis, and the inhibitor L-NAME attenuated the inhibition of ICAM-1 expression. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The effect runs through the nitric oxide enzyme the vessel wall makes. organism: Human and bovine cells tissue_or_cell_type: Vascular endothelium experimental_model: Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model limitations: An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route. exposure: Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME evidence_span: {"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"} [hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292