Zinc

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets

exposure

Cells cultured under experimental zinc-deficient conditions; depletion method and concentrations not specified in the abstract.

limitations

Abstract-only extraction. Individual enzyme-reaction assignments, depletion concentrations/durations, quantitative effects and human clinical implications are not established here. Hydrolysis of extracellular vitamin phosphates is distinct from intracellular cofactor activation.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Cell species not specified in abstract

plain_language

Low zinc availability reduced the experimental preparations’ ability to remove phosphate groups from B vitamins.

primary_references

[zinc-enz-bvitamins2024] Rate of hydrolysis of the phosphate esters of B vitamins is reduced by zinc deficiency: In vitro and in vivo. (2024). https://pubmed.ncbi.nlm.nih.gov/39279493/ DOI: 10.1096/fj.202401207r

tissue_or_cell_type

Cultured-cell membrane lysates

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 833–844

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets · source_derived_draft · unverified_draft

### zinc-enz-bvitamin-cell-hydrolysis Membrane lysates from cells cultured under zinc-deficient conditions had reduced extracellular B-vitamin phosphate-ester hydrolysis activity in the study. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low zinc availability reduced the experimental preparations’ ability to remove phosphate groups from B vitamins. organism: Cell species not specified in abstract tissue_or_cell_type: Cultured-cell membrane lysates experimental_model: Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets limitations: Abstract-only extraction. Individual enzyme-reaction assignments, depletion concentrations/durations, quantitative effects and human clinical implications are not established here. Hydrolysis of extracellular vitamin phosphates is distinct from intracellular cofactor activation. exposure: Cells cultured under experimental zinc-deficient conditions; depletion method and concentrations not specified in the abstract. cross_nutrient: true [zinc-enz-bvitamins2024] Rate of hydrolysis of the phosphate esters of B vitamins is reduced by zinc deficiency: In vitro and in vivo. (2024). https://pubmed.ncbi.nlm.nih.gov/39279493/ DOI: 10.1096/fj.202401207r

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

true

experimental_model

Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets

exposure

Rats fed zinc-deficient diets; dietary content and duration not available in the abstract.

limitations

Abstract-only extraction. Individual enzyme-reaction assignments, depletion concentrations/durations, quantitative effects and human clinical implications are not established here. Hydrolysis of extracellular vitamin phosphates is distinct from intracellular cofactor activation. The abstract does not identify which vitamin-specific endpoints were measurable in rat serum. The full-text search extract specifically said rat-serum B6 hydrolysis could not be measured; no rat B6 reaction claim or PLP participant is imported.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

Dietary zinc deficiency also reduced this measured enzyme activity in rat serum.

primary_references

[zinc-enz-bvitamins2024] Rate of hydrolysis of the phosphate esters of B vitamins is reduced by zinc deficiency: In vitro and in vivo. (2024). https://pubmed.ncbi.nlm.nih.gov/39279493/ DOI: 10.1096/fj.202401207r

tissue_or_cell_type

Rat serum assayed ex vivo

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 846–857

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets · source_derived_draft · unverified_draft

### zinc-enz-bvitamin-rat-hydrolysis Serum from rats fed zinc-deficient diets showed reduced B-vitamin phosphate-ester hydrolysis activity in the study. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Dietary zinc deficiency also reduced this measured enzyme activity in rat serum. organism: Rattus norvegicus tissue_or_cell_type: Rat serum assayed ex vivo experimental_model: Membrane lysates of transiently transfected or endogenously expressing cells; serum of rats fed zinc-deficient diets limitations: Abstract-only extraction. Individual enzyme-reaction assignments, depletion concentrations/durations, quantitative effects and human clinical implications are not established here. Hydrolysis of extracellular vitamin phosphates is distinct from intracellular cofactor activation. The abstract does not identify which vitamin-specific endpoints were measurable in rat serum. The full-text search extract specifically said rat-serum B6 hydrolysis could not be measured; no rat B6 reaction claim or PLP participant is imported. exposure: Rats fed zinc-deficient diets; dietary content and duration not available in the abstract. cross_nutrient: true [zinc-enz-bvitamins2024] Rate of hydrolysis of the phosphate esters of B vitamins is reduced by zinc deficiency: In vitro and in vivo. (2024). https://pubmed.ncbi.nlm.nih.gov/39279493/ DOI: 10.1096/fj.202401207r

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Controlled pregnancy diets and placental RNA/protein assays

exposure

15 versus 50 mg zinc/kg diet from pregnancy onset to day 17; 150 mg/kg group also had lower expression than 50 mg/kg.

limitations

Nonmonotonic expression must not be converted into a monotonic transport-flux model. These mouse diets are not human dose instructions or serum thresholds.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Mus musculus

plain_language

Moderately restricting maternal dietary zinc lowered placental ZnT1 in mice.

primary_references

[zinc-trans-16914197] Zinc transporters in the mouse placenta show a coordinated regulatory response to changes in dietary zinc intake. (2007). https://pubmed.ncbi.nlm.nih.gov/16914197/ DOI: 10.1016/j.placenta.2006.07.002

tissue_or_cell_type

Placenta

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 544–555

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled pregnancy diets and placental RNA/protein assays · source_derived_draft · unverified_draft

### zinc-trans-placenta-znt1-restriction Placental ZnT1 expression was lower in pregnant mice fed 15 mg zinc/kg diet than in those fed 50 mg/kg; the mRNA pattern was reflected at the protein level. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Moderately restricting maternal dietary zinc lowered placental ZnT1 in mice. organism: Mus musculus tissue_or_cell_type: Placenta experimental_model: Controlled pregnancy diets and placental RNA/protein assays limitations: Nonmonotonic expression must not be converted into a monotonic transport-flux model. These mouse diets are not human dose instructions or serum thresholds. exposure: 15 versus 50 mg zinc/kg diet from pregnancy onset to day 17; 150 mg/kg group also had lower expression than 50 mg/kg. cross_nutrient: false [zinc-trans-16914197] Zinc transporters in the mouse placenta show a coordinated regulatory response to changes in dietary zinc intake. (2007). https://pubmed.ncbi.nlm.nih.gov/16914197/ DOI: 10.1016/j.placenta.2006.07.002

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses

exposure

Defined zinc-deficient versus adequate diets; transcription assessed after 24 hours from gestational day 8.

limitations

Transcript stabilization in mice is not a serum-zinc threshold or proof that all zinc deficiency responses are post-transcriptional.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Mus musculus

plain_language

With little dietary zinc, mice preserve the message used to make ZIP4.

primary_references

[zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149

tissue_or_cell_type

Small intestine; supporting cultured hepatic cells

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 232–243

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses · source_derived_draft · unverified_draft

### zinc-trans-zip4-mrna-stability Dietary zinc deficiency increased mouse Zip4 mRNA by greater transcript stability rather than an increased relative transcription rate. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: With little dietary zinc, mice preserve the message used to make ZIP4. organism: Mus musculus tissue_or_cell_type: Small intestine; supporting cultured hepatic cells experimental_model: Mouse intestine with nuclear run-on assays; supporting Hepa-cell analyses limitations: Transcript stabilization in mice is not a serum-zinc threshold or proof that all zinc deficiency responses are post-transcriptional. exposure: Defined zinc-deficient versus adequate diets; transcription assessed after 24 hours from gestational day 8. cross_nutrient: false [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Dietary depletion/repletion and protein/RNA assays

exposure

Defined zinc-deficient diet followed in some experiments by oral zinc repletion.

limitations

Protein abundance, transcription and transport flux are different endpoints; this is a mouse dietary adaptation.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Mus musculus

plain_language

Zinc deficiency reduced ZIP5 protein without reducing its messenger RNA.

primary_references

[zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149

tissue_or_cell_type

Enterocytes, acinar cells and visceral endoderm

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 414–425

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary depletion/repletion and protein/RNA assays · source_derived_draft · unverified_draft

### zinc-trans-zip5-diet-deficiency During dietary zinc deficiency in mice, ZIP5 protein was internalized and degraded in enterocytes, pancreatic acinar cells and visceral endoderm even though Zip5 mRNA abundance did not change. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc deficiency reduced ZIP5 protein without reducing its messenger RNA. organism: Mus musculus tissue_or_cell_type: Enterocytes, acinar cells and visceral endoderm experimental_model: Dietary depletion/repletion and protein/RNA assays limitations: Protein abundance, transcription and transport flux are different endpoints; this is a mouse dietary adaptation. exposure: Defined zinc-deficient diet followed in some experiments by oral zinc repletion. cross_nutrient: false [zinc-trans-18020946] Novel zinc-responsive post-transcriptional mechanisms reciprocally regulate expression of the mouse Slc39a4 and Slc39a5 zinc transporters (Zip4 and Zip5). (2007). https://pubmed.ncbi.nlm.nih.gov/18020946/ DOI: 10.1515/bc.2007.149

cross_nutrient

Phytic acid / phytate (dietary_modifier)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/hunt2008.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "da28b136fa7271f3406a8cf55cc3e613a5e8749578c1ee662057ebe564df8995", "utf8_bytes": 1647}

experimental_model

Three controlled dietary experiments in 109 healthy adults

exposure

Ten diets: 4–29 mg zinc/day, phytate:zinc molar ratios 2–7 or 15–23, before and after 4 or 8 weeks.

limitations

Dietary restriction and adaptation are not proof of clinical zinc deficiency. The reported 92% was an upper observed absorption value, not a mean.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Zinc uptake can adapt to intake, but phytate constrained that adaptation.

primary_references

[zn-clin-hunt2008] Adaptation in human zinc absorption as influenced by dietary zinc and bioavailability. (2008). https://pubmed.ncbi.nlm.nih.gov/18469257/ DOI: 10.1093/ajcn/87.5.1336

tissue_or_cell_type

Intestinal absorption and candidate blood biomarkers

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1317–1330

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three controlled dietary experiments in 109 healthy adults · source_derived_draft · unverified_draft

### zn-clin-adaptation Absorption efficiency increased as dietary zinc fell. After 4–8 weeks below 11 mg zinc/day, further adaptation reached as high as 92% absorption on low-phytate diets; this additional adaptation was absent on high-phytate diets. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc uptake can adapt to intake, but phytate constrained that adaptation. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption and candidate blood biomarkers experimental_model: Three controlled dietary experiments in 109 healthy adults limitations: Dietary restriction and adaptation are not proof of clinical zinc deficiency. The reported 92% was an upper observed absorption value, not a mean. exposure: Ten diets: 4–29 mg zinc/day, phytate:zinc molar ratios 2–7 or 15–23, before and after 4 or 8 weeks. cross_nutrient: Phytic acid / phytate (dietary_modifier) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/hunt2008.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "da28b136fa7271f3406a8cf55cc3e613a5e8749578c1ee662057ebe564df8995", "utf8_bytes": 1647} [zn-clin-hunt2008] Adaptation in human zinc absorption as influenced by dietary zinc and bioavailability. (2008). https://pubmed.ncbi.nlm.nih.gov/18469257/ DOI: 10.1093/ajcn/87.5.1336

cross_nutrient

Zinc exposure and the specifically measured response.

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/hunt2008.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "da28b136fa7271f3406a8cf55cc3e613a5e8749578c1ee662057ebe564df8995", "utf8_bytes": 1647}

experimental_model

Three controlled dietary experiments in 109 healthy adults

exposure

Ten diets: 4–29 mg zinc/day, phytate:zinc molar ratios 2–7 or 15–23, before and after 4 or 8 weeks.

limitations

Dietary restriction and adaptation are not proof of clinical zinc deficiency. The reported 92% was an upper observed absorption value, not a mean.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Several candidate blood tests missed the dietary differences.

primary_references

[zn-clin-hunt2008] Adaptation in human zinc absorption as influenced by dietary zinc and bioavailability. (2008). https://pubmed.ncbi.nlm.nih.gov/18469257/ DOI: 10.1093/ajcn/87.5.1336

tissue_or_cell_type

Intestinal absorption and candidate blood biomarkers

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1332–1345

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three controlled dietary experiments in 109 healthy adults · source_derived_draft · unverified_draft

### zn-clin-adaptation-markers Erythrocyte osmotic fragility, in-vitro erythrocyte 65Zn uptake, and leukocyte ZIP1 and ZnT1 expression did not respond to dietary zinc content in these experiments. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Several candidate blood tests missed the dietary differences. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption and candidate blood biomarkers experimental_model: Three controlled dietary experiments in 109 healthy adults limitations: Dietary restriction and adaptation are not proof of clinical zinc deficiency. The reported 92% was an upper observed absorption value, not a mean. exposure: Ten diets: 4–29 mg zinc/day, phytate:zinc molar ratios 2–7 or 15–23, before and after 4 or 8 weeks. cross_nutrient: Zinc exposure and the specifically measured response. evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/hunt2008.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "da28b136fa7271f3406a8cf55cc3e613a5e8749578c1ee662057ebe564df8995", "utf8_bytes": 1647} [zn-clin-hunt2008] Adaptation in human zinc absorption as influenced by dietary zinc and bioavailability. (2008). https://pubmed.ncbi.nlm.nih.gov/18469257/ DOI: 10.1093/ajcn/87.5.1336

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Interferon gamma (measured_cytokine)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}

experimental_model

Experimental dietary zinc restriction and repletion in humans

exposure

Baseline, end of zinc restriction, and following repletion were assessed.

limitations

Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Zinc shortage reduced interferon gamma production in the tested immune cells.

primary_references

[zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

tissue_or_cell_type

T lymphocytes and cytokine production

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1347–1360

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

### zn-clin-depletion-ifng Experimental human zinc restriction reduced interferon gamma production, contributing to the selective decline in the tested TH1-associated cytokine response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage reduced interferon gamma production in the tested immune cells. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: Interferon gamma (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

interleukin-2 (measured_cytokine)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}

experimental_model

Experimental dietary zinc restriction and repletion in humans

exposure

Baseline, end of zinc restriction, and following repletion were assessed.

limitations

Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Zinc shortage reduced interleukin-2 production in the tested immune cells.

primary_references

[zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

tissue_or_cell_type

T lymphocytes and cytokine production

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1362–1375

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

### zn-clin-depletion-il2 Experimental human zinc restriction reduced interleukin-2 production, contributing to the selective decline in the tested TH1-associated cytokine response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage reduced interleukin-2 production in the tested immune cells. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: interleukin-2 (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Interleukin 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (measured_cytokine)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}

experimental_model

Experimental dietary zinc restriction and repletion in humans

exposure

Baseline, end of zinc restriction, and following repletion were assessed.

limitations

Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Zinc shortage did not suppress every cytokine in the same way.

primary_references

[zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

tissue_or_cell_type

T lymphocytes and cytokine production

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1392–1405

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

### zn-clin-depletion-th2-null Production of IL4, IL6 and IL10 was unchanged during the reported zinc-deficiency experiment, unlike the TH1-associated cytokines. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage did not suppress every cytokine in the same way. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: Interleukin 4 (measured_cytokine); interleukin 6 (measured_cytokine); Interleukin 10 (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Tumor necrosis factor (measured_cytokine)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106}

experimental_model

Experimental dietary zinc restriction and repletion in humans

exposure

Baseline, end of zinc restriction, and following repletion were assessed.

limitations

Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Zinc shortage reduced tumor necrosis factor alpha production in the tested immune cells.

primary_references

[zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

tissue_or_cell_type

T lymphocytes and cytokine production

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1377–1390

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Experimental dietary zinc restriction and repletion in humans · source_derived_draft · unverified_draft

### zn-clin-depletion-tnf Experimental human zinc restriction reduced tumor necrosis factor alpha production, contributing to the selective decline in the tested TH1-associated cytokine response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc shortage reduced tumor necrosis factor alpha production in the tested immune cells. organism: Homo sapiens tissue_or_cell_type: T lymphocytes and cytokine production experimental_model: Experimental dietary zinc restriction and repletion in humans limitations: Indexed abstract only; no sample size, intake, duration, assay stimulus or repletion effect size is invented. Changes in selected cytokines do not quantify overall infection risk. exposure: Baseline, end of zinc restriction, and following repletion were assessed. cross_nutrient: Tumor necrosis factor (measured_cytokine) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/beck1997.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "f731be20460b3ded18a253c1d1595c48849db9c09ef164f8a7d03a552e5619dd", "utf8_bytes": 1106} [zn-clin-beck1997] Changes in cytokine production and T cell subpopulations in experimentally induced zinc-deficient humans. (1997). https://pubmed.ncbi.nlm.nih.gov/9227444/ DOI: 10.1152/ajpendo.1997.272.6.e1002

cross_nutrient

Zinc exposure and the specifically measured response.

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/sazawal1995.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "8c21c0c3ec6dedca7f245298445dfe9f71d64ff618734cd66b0eac35952c5bc8", "utf8_bytes": 2090}

experimental_model

Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi

exposure

20 mg elemental zinc/day; all children received oral rehydration and vitamin supplements.

limitations

Not every child had confirmed zinc deficiency. Specific zinc salt is not verified from abstract; efficacy belongs to this regimen and background care.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

The zinc group recovered sooner, with differences depending on treatment timing.

primary_references

[zn-clin-sazawal1995] Zinc supplementation in young children with acute diarrhea in India. (1995). https://pubmed.ncbi.nlm.nih.gov/7651474/ DOI: 10.1056/nejm199509283331304

tissue_or_cell_type

Acute diarrheal illness

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1482–1495

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi · source_derived_draft · unverified_draft

### zn-clin-diarrhea-duration Zinc reduced continued-diarrhea risk by 23% (95% CI 12–32%); the reduction was 7% (−9 to 22%) on days 1–3 and 38% (27–48%) thereafter. Starting within three days reduced episodes lasting over seven days by 39% (7–61%). Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: The zinc group recovered sooner, with differences depending on treatment timing. organism: Homo sapiens tissue_or_cell_type: Acute diarrheal illness experimental_model: Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi limitations: Not every child had confirmed zinc deficiency. Specific zinc salt is not verified from abstract; efficacy belongs to this regimen and background care. exposure: 20 mg elemental zinc/day; all children received oral rehydration and vitamin supplements. cross_nutrient: Zinc exposure and the specifically measured response. evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/sazawal1995.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "8c21c0c3ec6dedca7f245298445dfe9f71d64ff618734cd66b0eac35952c5bc8", "utf8_bytes": 2090} [zn-clin-sazawal1995] Zinc supplementation in young children with acute diarrhea in India. (1995). https://pubmed.ncbi.nlm.nih.gov/7651474/ DOI: 10.1056/nejm199509283331304

cross_nutrient

Child diarrheal illness days (additional_endpoint)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/sazawal1995.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "8c21c0c3ec6dedca7f245298445dfe9f71d64ff618734cd66b0eac35952c5bc8", "utf8_bytes": 2090}

experimental_model

Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi

exposure

20 mg elemental zinc/day; all children received oral rehydration and vitamin supplements.

limitations

Not every child had confirmed zinc deficiency. Specific zinc salt is not verified from abstract; efficacy belongs to this regimen and background care.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

The trial found fewer watery stools as well as shorter illness.

primary_references

[zn-clin-sazawal1995] Zinc supplementation in young children with acute diarrhea in India. (1995). https://pubmed.ncbi.nlm.nih.gov/7651474/ DOI: 10.1056/nejm199509283331304

tissue_or_cell_type

Acute diarrheal illness

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1497–1510

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi · source_derived_draft · unverified_draft

### zn-clin-diarrhea-stools Mean watery stools per day fell by 39% (95% CI 6–70%; P=.02), and days with watery diarrhea by 21% (10–31%) in the zinc group. Benefits were larger in stunted children. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial found fewer watery stools as well as shorter illness. organism: Homo sapiens tissue_or_cell_type: Acute diarrheal illness experimental_model: Double-blind randomized controlled trial in 937 children aged 6–35 months in New Delhi limitations: Not every child had confirmed zinc deficiency. Specific zinc salt is not verified from abstract; efficacy belongs to this regimen and background care. exposure: 20 mg elemental zinc/day; all children received oral rehydration and vitamin supplements. cross_nutrient: Child diarrheal illness days (additional_endpoint) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/sazawal1995.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "8c21c0c3ec6dedca7f245298445dfe9f71d64ff618734cd66b0eac35952c5bc8", "utf8_bytes": 2090} [zn-clin-sazawal1995] Zinc supplementation in young children with acute diarrhea in India. (1995). https://pubmed.ncbi.nlm.nih.gov/7651474/ DOI: 10.1056/nejm199509283331304

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Copper (deficient_nutrient); Erythrocyte mean cell volume (reduced_endpoint); Blood neutrophil count (reduced_endpoint); Serum ceruloplasmin concentration (associated_marker)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487}

experimental_model

Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy

exposure

Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered.

limitations

Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Long zinc treatment was associated with copper shortage and blood-cell changes.

primary_references

[zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019

tissue_or_cell_type

Blood copper and hematology

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1407–1420

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy · source_derived_draft · unverified_draft

### zn-clin-hypocupremia An adult with sickle cell anemia developed hypocupremia after two years of zinc therapy, accompanied by microcytosis and relative neutropenia. Additional zinc-treated patients had varying hypoceruloplasminemia. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Long zinc treatment was associated with copper shortage and blood-cell changes. organism: Homo sapiens tissue_or_cell_type: Blood copper and hematology experimental_model: Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy limitations: Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio. exposure: Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered. cross_nutrient: Copper (deficient_nutrient); Erythrocyte mean cell volume (reduced_endpoint); Blood neutrophil count (reduced_endpoint); Serum ceruloplasmin concentration (associated_marker) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487} [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

Zinc exposure and the specifically measured response.

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/walker1973.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "350425d75c9023c5b9ddb97d734e320b4e07c6fe5b834213defb1adc7cc26b00", "utf8_bytes": 991}

experimental_model

Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients

exposure

Fasting and post-meal plasma samples; disease-group comparisons.

limitations

Correlations cannot distinguish dietary shortage from albumin binding, redistribution and disease effects. Plasma measurements are not intracellular zinc thresholds.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Blood sampling time and disease context changed the measured zinc level.

primary_references

[zn-clin-walker1973] Plasma and urinary zinc in patients with malabsorption syndromes or hepatic cirrhosis. (1973). https://pubmed.ncbi.nlm.nih.gov/4785284/ DOI: 10.1136/gut.14.12.943

tissue_or_cell_type

Plasma and urine

trigger_kind

biomarker_context Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1437–1450

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients · source_derived_draft · unverified_draft

### zn-clin-plasma-meals Fasting/post-meal plasma zinc means were 71/60 µg per 100 mL in cirrhosis, 76/64 in malabsorption and 97/81 in controls; the study also documented diurnal variation. Condition category: biomarker_context nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood sampling time and disease context changed the measured zinc level. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients limitations: Correlations cannot distinguish dietary shortage from albumin binding, redistribution and disease effects. Plasma measurements are not intracellular zinc thresholds. exposure: Fasting and post-meal plasma samples; disease-group comparisons. cross_nutrient: Zinc exposure and the specifically measured response. evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/walker1973.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "350425d75c9023c5b9ddb97d734e320b4e07c6fe5b834213defb1adc7cc26b00", "utf8_bytes": 991} [zn-clin-walker1973] Plasma and urinary zinc in patients with malabsorption syndromes or hepatic cirrhosis. (1973). https://pubmed.ncbi.nlm.nih.gov/4785284/ DOI: 10.1136/gut.14.12.943

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

Zinc exposure and the specifically measured response.

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/walker1973.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "350425d75c9023c5b9ddb97d734e320b4e07c6fe5b834213defb1adc7cc26b00", "utf8_bytes": 991}

experimental_model

Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients

exposure

Fasting and post-meal plasma samples; disease-group comparisons.

limitations

Correlations cannot distinguish dietary shortage from albumin binding, redistribution and disease effects. Plasma measurements are not intracellular zinc thresholds.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Similar plasma results did not imply the same route of zinc loss.

primary_references

[zn-clin-walker1973] Plasma and urinary zinc in patients with malabsorption syndromes or hepatic cirrhosis. (1973). https://pubmed.ncbi.nlm.nih.gov/4785284/ DOI: 10.1136/gut.14.12.943

tissue_or_cell_type

Plasma and urine

trigger_kind

biomarker_context Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1467–1480

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients · source_derived_draft · unverified_draft

### zn-clin-urinary-loss Urinary zinc excretion was increased in cirrhosis but not in malabsorption, although both groups had low plasma zinc. Condition category: biomarker_context nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Similar plasma results did not imply the same route of zinc loss. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Observational comparison of 19 malabsorption patients, 21 cirrhosis patients, 20 controls and 23 other disease patients limitations: Correlations cannot distinguish dietary shortage from albumin binding, redistribution and disease effects. Plasma measurements are not intracellular zinc thresholds. exposure: Fasting and post-meal plasma samples; disease-group comparisons. cross_nutrient: Zinc exposure and the specifically measured response. evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/walker1973.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "350425d75c9023c5b9ddb97d734e320b4e07c6fe5b834213defb1adc7cc26b00", "utf8_bytes": 991} [zn-clin-walker1973] Plasma and urinary zinc in patients with malabsorption syndromes or hepatic cirrhosis. (1973). https://pubmed.ncbi.nlm.nih.gov/4785284/ DOI: 10.1136/gut.14.12.943

cross_nutrient

Copper (retained_nutrient); Copper bound to rat intestinal metallothioneins (retained_complex)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"}

experimental_model

Dietary radiotracer experiments in rats

exposure

High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements.

limitations

High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

Induced binding proteins provide a mechanism for retaining copper in the gut.

primary_references

[zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

tissue_or_cell_type

Small intestine

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 915–927

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary radiotracer experiments in rats · source_derived_draft · unverified_draft

### zn-sig-copper-mt-retention The increased intestinal 64Cu was predominantly metallothionein-associated; the authors inferred copper displacement of zinc after zinc-induced metallothionein synthesis. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Induced binding proteins provide a mechanism for retaining copper in the gut. organism: Rattus norvegicus tissue_or_cell_type: Small intestine experimental_model: Dietary radiotracer experiments in rats limitations: High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation. exposure: High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements. cross_nutrient: Copper (retained_nutrient); Copper bound to rat intestinal metallothioneins (retained_complex) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"} [zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Zinc(II) ion (availability_modifier)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/16892068-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "922aedddf1d5d49fc62e39285307917b93201e23b5b7ea57a60136edd6762a17"}

experimental_model

Dendritic-cell signaling study

exposure

Experimental zinc chelation, not dietary zinc restriction. Chelator identity, concentration and exposure time are not verified in the indexed abstract.

limitations

Chelation is a manipulation of available cellular zinc. It is not evidence for a human intake threshold or a universal immune benefit of low zinc.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Mus musculus

plain_language

Experimentally binding available zinc reproduced part of the dendritic-cell response.

primary_references

[zn-sig-16892068] Toll-like receptor-mediated regulation of zinc homeostasis influences dendritic cell function. (2006). https://pubmed.ncbi.nlm.nih.gov/16892068/ DOI: 10.1038/ni1373

tissue_or_cell_type

Dendritic cells

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1167–1179

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dendritic-cell signaling study · source_derived_draft · unverified_draft

### zn-sig-dendritic-chelation A zinc chelator mimicked the dendritic-cell effects of LPS in the primary study, which linked reduced intracellular free zinc to the maturation-marker response. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Experimentally binding available zinc reproduced part of the dendritic-cell response. organism: Mus musculus tissue_or_cell_type: Dendritic cells experimental_model: Dendritic-cell signaling study limitations: Chelation is a manipulation of available cellular zinc. It is not evidence for a human intake threshold or a universal immune benefit of low zinc. exposure: Experimental zinc chelation, not dietary zinc restriction. Chelator identity, concentration and exposure time are not verified in the indexed abstract. cross_nutrient: Zinc(II) ion (availability_modifier) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/16892068-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "922aedddf1d5d49fc62e39285307917b93201e23b5b7ea57a60136edd6762a17"} [zn-sig-16892068] Toll-like receptor-mediated regulation of zinc homeostasis influences dendritic cell function. (2006). https://pubmed.ncbi.nlm.nih.gov/16892068/ DOI: 10.1038/ni1373

cross_nutrient

Copper (affected_nutrient)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"}

experimental_model

Isolated vascularly perfused intestine from diet-conditioned rats

exposure

Dietary copper/zinc variation for one week versus direct luminal-metal variation.

limitations

Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

At high luminal exposure, copper entry or transfer was inhibited.

primary_references

[zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

tissue_or_cell_type

Small-intestinal mucosa and portal effluent

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 957–969

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated vascularly perfused intestine from diet-conditioned rats · source_derived_draft · unverified_draft

### zn-sig-luminal-zinc-copper High luminal zinc reduced both mucosal cytosolic copper and copper transfer into portal effluent in the perfused-rat-intestine experiments. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: At high luminal exposure, copper entry or transfer was inhibited. organism: Rattus norvegicus tissue_or_cell_type: Small-intestinal mucosa and portal effluent experimental_model: Isolated vascularly perfused intestine from diet-conditioned rats limitations: Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption. exposure: Dietary copper/zinc variation for one week versus direct luminal-metal variation. cross_nutrient: Copper (affected_nutrient) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"} [zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

cross_nutrient

Copper (affected_nutrient); Intestinal copper absorption (unchanged_endpoint); Rat intestinal metallothioneins measured without isoform resolution (binding_proteins)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"}

experimental_model

Isolated vascularly perfused intestine from diet-conditioned rats

exposure

Dietary copper/zinc variation for one week versus direct luminal-metal variation.

limitations

Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

More copper on a binding protein did not always mean less copper absorption.

primary_references

[zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

tissue_or_cell_type

Small-intestinal mucosa and portal effluent

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 943–955

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated vascularly perfused intestine from diet-conditioned rats · source_derived_draft · unverified_draft

### zn-sig-mt-binding-not-absorption After the tested dietary conditioning, high zinc increased metallothionein-bound copper without changing intracellular copper concentration or significantly altering measured copper absorption in the perfused intestine. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: More copper on a binding protein did not always mean less copper absorption. organism: Rattus norvegicus tissue_or_cell_type: Small-intestinal mucosa and portal effluent experimental_model: Isolated vascularly perfused intestine from diet-conditioned rats limitations: Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption. exposure: Dietary copper/zinc variation for one week versus direct luminal-metal variation. cross_nutrient: Copper (affected_nutrient); Intestinal copper absorption (unchanged_endpoint); Rat intestinal metallothioneins measured without isoform resolution (binding_proteins) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"} [zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

cross_nutrient

Copper (affected_nutrient); Intestinal mucosal copper retention (increased_endpoint)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"}

experimental_model

Dietary radiotracer experiments in rats

exposure

High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements.

limitations

High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

Very high zinc trapped more copper in the intestine while less was absorbed.

primary_references

[zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

tissue_or_cell_type

Small intestine

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 901–913

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary radiotracer experiments in rats · source_derived_draft · unverified_draft

### zn-sig-zinc-copper-absorption Rat diets with zinc up to 450 mg/kg did not change 64Cu absorption; 900 mg/kg reduced it by about 40% and increased mucosal 64Cu uptake. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Very high zinc trapped more copper in the intestine while less was absorbed. organism: Rattus norvegicus tissue_or_cell_type: Small intestine experimental_model: Dietary radiotracer experiments in rats limitations: High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation. exposure: High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements. cross_nutrient: Copper (affected_nutrient); Intestinal mucosal copper retention (increased_endpoint) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"} [zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Mouse ZIP7 / Slc39a7 (affected_transporter)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"}

experimental_model

Conditional intestinal Zip7-deficient mice and organoids

exposure

Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction.

limitations

Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Mus musculus

plain_language

More available zinc did not substitute for the missing distribution machinery.

primary_references

[zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349

tissue_or_cell_type

Intestinal crypts, progenitor cells and organoids

trigger_kind

machinery_impairment Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1139–1151

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Zip7-deficient mice and organoids · source_derived_draft · unverified_draft

### zn-sig-zip7-zinc-no-rescue Adding 1 µM ZnSO4 did not suppress ER-stress gene induction in Zip7-deficient intestinal organoids assessed 48 hours after induction of deletion; the study also observed no rescue in fibroblasts, while restored ZIP7 expression rescued their stress response. Condition category: machinery_impairment nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: More available zinc did not substitute for the missing distribution machinery. organism: Mus musculus tissue_or_cell_type: Intestinal crypts, progenitor cells and organoids experimental_model: Conditional intestinal Zip7-deficient mice and organoids limitations: Cell lineage and tissue context matter. Supplementation failing to rescue a transporter defect is not evidence that ordinary dietary zinc replacement fails. exposure: Supplemental Figure S8: 1 µM ZnSO4; intestinal organoids assessed 48 hours after the study-induced Zip7 deletion. The fibroblast comparison also used 1 µM ZnSO4. This exposure did not suppress the measured ER-stress gene induction. cross_nutrient: Mouse ZIP7 / Slc39a7 (affected_transporter) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/27736879.txt", "locator": "Results: Zip7 deletion activates ER stress; Figure 4, Figure 5 and supplemental Figure S8", "file_sha256": "4771f8b4a2b4e332b10bd2a5abef6f538cc38f4c85916b44ddab9f15679ed621"} [zn-sig-27736879] Zinc Transporter SLC39A7/ZIP7 Promotes Intestinal Epithelial Self-Renewal by Resolving ER Stress. (2016). https://pubmed.ncbi.nlm.nih.gov/27736879/ DOI: 10.1371/journal.pgen.1006349

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Zinc -> hepatic retinoid metabolism.

experimental_model

Pair-feeding controls; three weeks.

limitations

Does not show that every retinol dehydrogenase is a zinc enzyme.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Rattus norvegicus

plain_language

Zinc depletion changed retinoid handling in the liver.

primary_references

[va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995

tissue_or_cell_type

Liver

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1519–1529

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pair-feeding controls; three weeks. · source_derived_draft · unverified_draft

### va-zinc-deficiency-adh-decrease Zinc-deficient rats had lower hepatic retinol-oxidizing ADH activity and greater hepatic vitamin A content. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc depletion changed retinoid handling in the liver. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Pair-feeding controls; three weeks. limitations: Does not show that every retinol dehydrogenase is a zinc enzyme. cross_nutrient: Zinc -> hepatic retinoid metabolism. [va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995

availability_state

nutrient_deficiency Imported condition classification; unverified.

experimental_model

Same hepatic activity assays.

limitations

Activity is not whole-body flux or proof of a direct zinc-binding requirement.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Rattus norvegicus

plain_language

Vitamin A processing did not simply stop at every step.

primary_references

[va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995

tissue_or_cell_type

Liver

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1531–1540

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same hepatic activity assays. · source_derived_draft · unverified_draft

### va-zinc-deficiency-retinal-oxidation-increase The same zinc-deficient rats showed increased retinal oxidase activity, with no detected REH/ARAT activity changes. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A processing did not simply stop at every step. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Same hepatic activity assays. limitations: Activity is not whole-body flux or proof of a direct zinc-binding requirement. [va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995

cross_nutrient

Zinc -> vitamin A biomarkers.

experimental_model

Six-month preschool trial.

limitations

No direct proof of restored liver release or increased RBP synthesis.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Homo sapiens

plain_language

Zinc status can influence vitamin A transport-related blood measurements.

primary_references

[va-munoz2000] Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers (2000). https://pubmed.ncbi.nlm.nih.gov/10702174/ DOI: 10.1093/ajcn/71.3.789

tissue_or_cell_type

Plasma

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1483–1493

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month preschool trial. · source_derived_draft · unverified_draft

### va-zinc-improves-retinol-marker Zinc increased plasma retinol and transthyretin versus placebo; the RBP increase was not significant. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Zinc status can influence vitamin A transport-related blood measurements. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Six-month preschool trial. limitations: No direct proof of restored liver release or increased RBP synthesis. cross_nutrient: Zinc -> vitamin A biomarkers. [va-munoz2000] Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers (2000). https://pubmed.ncbi.nlm.nih.gov/10702174/ DOI: 10.1093/ajcn/71.3.789

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Zinc/vitamin A -> dark-adaptation response.

experimental_model

Three-week zinc randomization, existing vitamin A allocation.

limitations

Not a universal zinc requirement; relative estimate had a wide confidence interval.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Homo sapiens

plain_language

An additional shortage may limit the response, but this result was subgroup-specific.

primary_references

[va-christian2001] Zinc supplementation might potentiate the effect of vitamin A in restoring night vision in pregnant Nepalese women (2001). https://pubmed.ncbi.nlm.nih.gov/11382658/ DOI: 10.1093/ajcn/73.6.1045

tissue_or_cell_type

Human visual function

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1507–1517

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-week zinc randomization, existing vitamin A allocation. · source_derived_draft · unverified_draft

### va-zinc-night-vision-subgroup In women with low initial zinc, vitamin A plus zinc improved night-vision recovery versus double placebo; zinc alone did not. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An additional shortage may limit the response, but this result was subgroup-specific. organism: Homo sapiens tissue_or_cell_type: Human visual function experimental_model: Three-week zinc randomization, existing vitamin A allocation. limitations: Not a universal zinc requirement; relative estimate had a wide confidence interval. cross_nutrient: Zinc/vitamin A -> dark-adaptation response. [va-christian2001] Zinc supplementation might potentiate the effect of vitamin A in restoring night vision in pregnant Nepalese women (2001). https://pubmed.ncbi.nlm.nih.gov/11382658/ DOI: 10.1093/ajcn/73.6.1045

evidence_span

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experimental_model

X-ray crystallography of horse liver alcohol dehydrogenase at 2.9 angstrom

exposure

Inhibitor-bound and coenzyme-bound states

limitations

The founding structure of the enzyme family, in horse liver enzyme. It establishes where the zinc and the coenzyme sit; it is not a human kinetic measurement.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Horse enzyme

plain_language

The zinc that does the chemistry sits at the bottom of a deep slot, far from the surface.

primary_references

[alcohol-p4365379] Structure of liver alcohol dehydrogenase at 2.9-angstrom resolution. (1973). https://pubmed.ncbi.nlm.nih.gov/4365379/ DOI: 10.1073/pnas.70.8.2439

tissue_or_cell_type

Purified dimeric enzyme

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 59–70

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray crystallography of horse liver alcohol dehydrogenase at 2.9 angstrom · source_derived_draft · unverified_draft

### alcohol-adh-catalytic-zinc-position Each subunit of the dimeric enzyme is organised into two unequal parts separated by a wide deep active-site cleft, with the catalytic zinc atoms bound at the bottom of the clefts about 20 angstrom from the molecular surface, and the adenosine moiety of the coenzyme bound within the smaller region. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The zinc that does the chemistry sits at the bottom of a deep slot, far from the surface. organism: Horse enzyme tissue_or_cell_type: Purified dimeric enzyme experimental_model: X-ray crystallography of horse liver alcohol dehydrogenase at 2.9 angstrom limitations: The founding structure of the enzyme family, in horse liver enzyme. It establishes where the zinc and the coenzyme sit; it is not a human kinetic measurement. exposure: Inhibitor-bound and coenzyme-bound states evidence_span: {"source_cache": "artifacts/alcohol-research/4365379.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "857dc9a65cac403f6591e0f33ea1bd3295f4a997274a26c362a3f392dbe9c987", "start_char": 0, "end_char": 912, "text_sha256": "857dc9a65cac403f6591e0f33ea1bd3295f4a997274a26c362a3f392dbe9c987"} [alcohol-p4365379] Structure of liver alcohol dehydrogenase at 2.9-angstrom resolution. (1973). https://pubmed.ncbi.nlm.nih.gov/4365379/ DOI: 10.1073/pnas.70.8.2439

evidence_span

{"source_cache": "artifacts/alcohol-research/25157460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c91a7069c53b4af61096bdc09ce952b0277d63d547a94e5d3870d2980aa31e20", "start_char": 0, "end_char": 1560, "text_sha256": "c91a7069c53b4af61096bdc09ce952b0277d63d547a94e5d3870d2980aa31e20"}

experimental_model

X-ray crystallography of yeast ADH1 at 2.4 angstrom with site-directed mutagenesis

exposure

Coenzyme-bound closed and open subunit conformations

limitations

A yeast enzyme, used because its asymmetric tetramer captures two catalytic states. The zinc coordination chemistry is conserved, but kinetic numbers are yeast numbers.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Yeast enzyme

plain_language

Three amino acids hold the zinc, and a fourth swings in to hand over the alcohol.

primary_references

[alcohol-p25157460] Yeast alcohol dehydrogenase structure and catalysis. (2014). https://pubmed.ncbi.nlm.nih.gov/25157460/ DOI: 10.1021/bi5006442

tissue_or_cell_type

Purified homotetramer

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 72–83

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray crystallography of yeast ADH1 at 2.4 angstrom with site-directed mutagenesis · source_derived_draft · unverified_draft

### alcohol-zinc-coordination-chemistry In the closed subunits the catalytic zinc holds the substrate oxygen in classical tetrahedral coordination with Cys-43, Cys-153 and His-66, while in the open subunits the zinc takes an inverted coordination that adds the carboxylate of Glu-67, which may be an intermediate in displacing the zinc-bound water with the alcohol substrate. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Three amino acids hold the zinc, and a fourth swings in to hand over the alcohol. organism: Yeast enzyme tissue_or_cell_type: Purified homotetramer experimental_model: X-ray crystallography of yeast ADH1 at 2.4 angstrom with site-directed mutagenesis limitations: A yeast enzyme, used because its asymmetric tetramer captures two catalytic states. The zinc coordination chemistry is conserved, but kinetic numbers are yeast numbers. exposure: Coenzyme-bound closed and open subunit conformations evidence_span: {"source_cache": "artifacts/alcohol-research/25157460.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c91a7069c53b4af61096bdc09ce952b0277d63d547a94e5d3870d2980aa31e20", "start_char": 0, "end_char": 1560, "text_sha256": "c91a7069c53b4af61096bdc09ce952b0277d63d547a94e5d3870d2980aa31e20"} [alcohol-p25157460] Yeast alcohol dehydrogenase structure and catalysis. (2014). https://pubmed.ncbi.nlm.nih.gov/25157460/ DOI: 10.1021/bi5006442

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/alcohol-research/15920153.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c25d41f17a1af981cc13b2e85ff6017ea8d48817b1fe8e4f22f8a3126e1af244", "start_char": 0, "end_char": 1654, "text_sha256": "c25d41f17a1af981cc13b2e85ff6017ea8d48817b1fe8e4f22f8a3126e1af244"}

experimental_model

Alcohol-fed mice given zinc supplementation with oxidative stress measurement

exposure

Chronic alcohol feeding with and without zinc supplementation

limitations

A repletion experiment, which is stronger than an association. It is a mouse prevention model, not a treatment trial.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Mouse

plain_language

Giving zinc back prevented the liver damage in this model.

primary_references

[alcohol-p15920153] Zinc supplementation prevents alcoholic liver injury in mice through attenuation of oxidative stress. (2005). https://pubmed.ncbi.nlm.nih.gov/15920153/ DOI: 10.1016/s0002-9440(10)62478-9

tissue_or_cell_type

Liver

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 787–798

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Alcohol-fed mice given zinc supplementation with oxidative stress measurement · source_derived_draft · unverified_draft

### alcohol-zinc-supplementation-liver Zinc supplementation prevented alcoholic liver injury in mice through attenuation of oxidative stress. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Giving zinc back prevented the liver damage in this model. organism: Mouse tissue_or_cell_type: Liver experimental_model: Alcohol-fed mice given zinc supplementation with oxidative stress measurement limitations: A repletion experiment, which is stronger than an association. It is a mouse prevention model, not a treatment trial. exposure: Chronic alcohol feeding with and without zinc supplementation evidence_span: {"source_cache": "artifacts/alcohol-research/15920153.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c25d41f17a1af981cc13b2e85ff6017ea8d48817b1fe8e4f22f8a3126e1af244", "start_char": 0, "end_char": 1654, "text_sha256": "c25d41f17a1af981cc13b2e85ff6017ea8d48817b1fe8e4f22f8a3126e1af244"} [alcohol-p15920153] Zinc supplementation prevents alcoholic liver injury in mice through attenuation of oxidative stress. (2005). https://pubmed.ncbi.nlm.nih.gov/15920153/ DOI: 10.1016/s0002-9440(10)62478-9

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation

exposure

Four weeks of alcohol liquid diet; zinc deprivation in culture

limitations

The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Mouse and human cells

plain_language

Take zinc away and the seals between cells come apart, with or without alcohol.

primary_references

[alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009

tissue_or_cell_type

Ileum and Caco-2 monolayers

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 774–785

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation · source_derived_draft · unverified_draft

### alcohol-zinc-tight-junctions Zinc deprivation caused epithelial barrier disruption in association with disassembly of tight junction proteins in Caco-2 monolayers, and minor zinc deprivation exaggerated the deleterious effect of alcohol on the epithelial barrier. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Take zinc away and the seals between cells come apart, with or without alcohol. organism: Mouse and human cells tissue_or_cell_type: Ileum and Caco-2 monolayers experimental_model: Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation limitations: The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells. exposure: Four weeks of alcohol liquid diet; zinc deprivation in culture evidence_span: {"source_cache": "artifacts/alcohol-research/20167873.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e", "start_char": 0, "end_char": 1542, "text_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e"} [alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009

evidence_span

{"source_cache": "artifacts/pectin-research/celus2018.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2ac4b4f67d7dfb4d68a06455691f949be93304d25c3475bd8caf4d618d96f472", "start_char": 0, "end_char": 1681, "text_sha256": "2ac4b4f67d7dfb4d68a06455691f949be93304d25c3475bd8caf4d618d96f472"}

experimental_model

Adsorption isotherms and simulated digestion

exposure

Citrus pectin with varied methylesterification and blockiness

limitations

In-vitro accessibility is not human mineral status.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

No organism; in-vitro food chemistry

plain_language

Pectin structure changes mineral binding.

primary_references

[pectin-pcelus2018] Interactions between citrus pectin and Zn2+ or Ca2+ and associated in vitro Zn2+ bioaccessibility as affected by degree of methylesterification and blockiness (2018). https://doi.org/10.1016/j.foodhyd.2018.01.003 DOI: 10.1016/j.foodhyd.2018.01.003

tissue_or_cell_type

Pectin-mineral solutions

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 490–501

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adsorption isotherms and simulated digestion · source_derived_draft · unverified_draft

### pectin-zinc-binding Lower methylesterification and greater blockiness favored zinc binding. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pectin structure changes mineral binding. organism: No organism; in-vitro food chemistry tissue_or_cell_type: Pectin-mineral solutions experimental_model: Adsorption isotherms and simulated digestion limitations: In-vitro accessibility is not human mineral status. exposure: Citrus pectin with varied methylesterification and blockiness evidence_span: {"source_cache": "artifacts/pectin-research/celus2018.publisher-abstract.txt", "locator": "Primary publisher abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2ac4b4f67d7dfb4d68a06455691f949be93304d25c3475bd8caf4d618d96f472", "start_char": 0, "end_char": 1681, "text_sha256": "2ac4b4f67d7dfb4d68a06455691f949be93304d25c3475bd8caf4d618d96f472"} [pectin-pcelus2018] Interactions between citrus pectin and Zn2+ or Ca2+ and associated in vitro Zn2+ bioaccessibility as affected by degree of methylesterification and blockiness (2018). https://doi.org/10.1016/j.foodhyd.2018.01.003 DOI: 10.1016/j.foodhyd.2018.01.003

availability_state

biomarker_context Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Human family/variant study; yeast functional validation of variants.

limitations

An association and one treatment observation do not establish how IARS dysfunction caused low zinc or that all isoleucine shortages deplete zinc.

nutrient_topic

L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine

plain_language

A coexisting nutrient shortage was documented in this rare genetic disorder.

primary_references

Biallelic IARS Mutations Cause Growth Retardation with Prenatal Onset, Intellectual Disability, Muscular Hypotonia, and Infantile Hepatopathy. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27426735/ · DOI 10.1016/j.ajhg.2016.05.027

trigger_kind

biomarker_context Imported condition classification; unverified.

L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 146–152

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family/variant study; yeast functional validation of variants. · source_derived_draft · unverified_draft

## isoleucine-iars-zinc-context A coexisting nutrient shortage was documented in this rare genetic disorder. Three individuals with biallelic IARS variants had zinc deficiency; one showed improved growth with zinc supplementation. Model: Human family/variant study; yeast functional validation of variants. Limitations: An association and one treatment observation do not establish how IARS dysfunction caused low zinc or that all isoleucine shortages deplete zinc. Evidence access: Primary abstract Biallelic IARS Mutations Cause Growth Retardation with Prenatal Onset, Intellectual Disability, Muscular Hypotonia, and Infantile Hepatopathy. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27426735/ · DOI 10.1016/j.ajhg.2016.05.027

evidence_span

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experimental_model

Zinc versus zinc-plus-iron intervention

exposure

50 mg/day zinc with or without 50 mg/day iron for ten weeks

limitations

Study exposures, not dosing recommendations; erythrocyte enzyme activity and ceruloplasmin concentration are distinct endpoints.

nutrient_topic

Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper

organism

Human adult females

plain_language

Correcting the iron side of an interaction did not correct the copper-related enzyme endpoint.

primary_references

[copper-p2912000] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145

tissue_or_cell_type

Erythrocytes and serum

Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1170–1181

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Zinc versus zinc-plus-iron intervention · source_derived_draft · unverified_draft

### copper-iron-does-not-prevent-zinc-sod-fall Adding iron to the zinc intervention prevented adverse iron-status changes but did not prevent the fall in erythrocyte Cu/Zn-SOD activity. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting the iron side of an interaction did not correct the copper-related enzyme endpoint. organism: Human adult females tissue_or_cell_type: Erythrocytes and serum experimental_model: Zinc versus zinc-plus-iron intervention limitations: Study exposures, not dosing recommendations; erythrocyte enzyme activity and ceruloplasmin concentration are distinct endpoints. exposure: 50 mg/day zinc with or without 50 mg/day iron for ten weeks evidence_span: {"source_cache": "artifacts/copper-research/2912000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443", "start_char": 0, "end_char": 969, "text_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443"} [copper-p2912000] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145

evidence_span

{"source_cache": "artifacts/melatonin-research/21226679.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2381a465728ea91061029d1d1d565623a15bdb941acf0cc9dbd2ed872fda32cf", "start_char": 0, "end_char": 1911, "text_sha256": "2381a465728ea91061029d1d1d565623a15bdb941acf0cc9dbd2ed872fda32cf"}

experimental_model

Double-blind placebo-controlled mixture trial

exposure

5 mg melatonin, 225 mg magnesium and 11.25 mg zinc nightly for eight weeks

limitations

Three active ingredients without separate ingredient arms; cannot demonstrate synergy or identify which ingredient caused the improvement. Single facility and short duration.

nutrient_topic

Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin

organism

43 elderly long-term-care residents with primary insomnia

plain_language

The tested product helped this outcome, but it does not isolate magnesium, zinc or melatonin.

primary_references

[melatonin-p21226679] The effect of melatonin, magnesium, and zinc on primary insomnia in long-term care facility residents in Italy: a double-blind, placebo-controlled clinical trial. (2011). https://pubmed.ncbi.nlm.nih.gov/21226679/ DOI: 10.1111/j.1532-5415.2010.03232.x

tissue_or_cell_type

Subjective and device-estimated sleep

Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 825–836

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind placebo-controlled mixture trial · source_derived_draft · unverified_draft

### melatonin-mg-zinc-mixture-sleep The combination improved global PSQI sleep-quality scores compared with placebo. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The tested product helped this outcome, but it does not isolate magnesium, zinc or melatonin. organism: 43 elderly long-term-care residents with primary insomnia tissue_or_cell_type: Subjective and device-estimated sleep experimental_model: Double-blind placebo-controlled mixture trial limitations: Three active ingredients without separate ingredient arms; cannot demonstrate synergy or identify which ingredient caused the improvement. Single facility and short duration. exposure: 5 mg melatonin, 225 mg magnesium and 11.25 mg zinc nightly for eight weeks evidence_span: {"source_cache": "artifacts/melatonin-research/21226679.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2381a465728ea91061029d1d1d565623a15bdb941acf0cc9dbd2ed872fda32cf", "start_char": 0, "end_char": 1911, "text_sha256": "2381a465728ea91061029d1d1d565623a15bdb941acf0cc9dbd2ed872fda32cf"} [melatonin-p21226679] The effect of melatonin, magnesium, and zinc on primary insomnia in long-term care facility residents in Italy: a double-blind, placebo-controlled clinical trial. (2011). https://pubmed.ncbi.nlm.nih.gov/21226679/ DOI: 10.1111/j.1532-5415.2010.03232.x

availability_state

machinery_impairment Imported condition classification; unverified.

curation_topic

zinc · Zinc

experimental_condition

Wild-type cells with the same TPEN exposure Limited availability during TPEN exposure · Zinc Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_condition

Wild-type cells with the same TPEN exposure Null genotype; R138X tested separately · Human zinc transporter ZnT8 / SLC30A8 Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "ZnT8 loss plus TPEN", "comparator": "Wild-type cells with the same TPEN exposure", "endpoint": "TUNEL-positive beta cells", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "slc30a8", "state": "Null genotype; R138X tested separately"}, {"entity_slug": "zinc", "state": "Limited availability during TPEN exposure"}]} Explicit extracted experimental comparison; source-derived draft.

experimental_model

Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed

limitations

Chelator challenge, not dietary restriction; human in-vivo protection by this mechanism remains untested.

primary_references

SLC30A8 stem-cell study; 2023; PMCID:PMC10047077; https://pmc.ncbi.nlm.nih.gov/articles/PMC10047077/

trigger_kind

machinery_impairment Imported condition classification; unverified.

Diabetes cascade: targeted primary-source supplement · lines 15–15

See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed · source_derived_draft · unverified_draft

After 5 micromolar TPEN for 48 hours, apoptosis was lower in SLC30A8-null and R138X cells than treated wild-type cells. Model: Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed. Limits: Chelator challenge, not dietary restriction; human in-vivo protection by this mechanism remains untested. Primary reference: SLC30A8 stem-cell study; 2023; PMCID:PMC10047077; https://pmc.ncbi.nlm.nih.gov/articles/PMC10047077/

availability_state

machinery_impairment Imported condition classification; unverified.

curation_topic

zinc · Zinc

experimental_condition

Wild-type cells SLC30A8 knockout · Human stem-cell-derived SLC30A8-null beta cells Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "SLC30A8 knockout", "comparator": "Wild-type cells", "endpoint": "Cytosolic free zinc", "effect_direction": "increase", "combination": "single", "conditions": [{"entity_slug": "human-slc30a8-null-beta-cells", "state": "SLC30A8 knockout"}]} Explicit extracted experimental comparison; source-derived draft.

experimental_model

Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed

limitations

Compartment-specific sensor measurement; not total-body zinc.

primary_references

SLC30A8 stem-cell study; 2023; PMCID:PMC10047077; https://pmc.ncbi.nlm.nih.gov/articles/PMC10047077/

trigger_kind

machinery_impairment Imported condition classification; unverified.

Diabetes cascade: targeted primary-source supplement · lines 9–9

See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed · source_derived_draft · unverified_draft

SLC30A8 knockout elevated free cytosolic zinc, whereas R138X did not show the same significant elevation. Model: Engineered human embryonic stem-cell-derived beta cells; results and figure 5 reviewed. Limits: Compartment-specific sensor measurement; not total-body zinc. Primary reference: SLC30A8 stem-cell study; 2023; PMCID:PMC10047077; https://pmc.ncbi.nlm.nih.gov/articles/PMC10047077/

availability_state

machinery_impairment Imported condition classification; unverified.

curation_topic

zinc · Zinc

experimental_condition

Noncarrier Truncating-variant carrier · Human SLC30A8 protein-truncating variant carrier state Condition belongs to the full experimental contrast; do not separate a joint intervention.

experimental_contrast

{"intervention": "Truncating-variant carrier", "comparator": "Noncarrier", "endpoint": "T2D risk", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "human-slc30a8-truncating-genotype", "state": "Truncating-variant carrier"}]} Explicit extracted experimental comparison; source-derived draft.

experimental_model

Human genetic association across five ancestry groups

limitations

Publisher abstract reviewed; genetic transporter loss is not dietary zinc restriction or a demonstrated supplement effect.

primary_references

Flannick et al. 2014; DOI:10.1038/ng.2915; PMCID:PMC4051628; https://www.nature.com/articles/ng.2915

trigger_kind

machinery_impairment Imported condition classification; unverified.

Diabetes cascade: targeted primary-source supplement · lines 6–6

See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Human genetic association across five ancestry groups · source_derived_draft · unverified_draft

Across approximately 150,000 people, carriers of 12 rare SLC30A8 truncating variants had 65% lower type 2 diabetes risk. Model: Human genetic association across five ancestry groups. Limits: Publisher abstract reviewed; genetic transporter loss is not dietary zinc restriction or a demonstrated supplement effect. Primary reference: Flannick et al. 2014; DOI:10.1038/ng.2915; PMCID:PMC4051628; https://www.nature.com/articles/ng.2915

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Human APIP mutant-function study.

limitations

Mutating a metal-binding site is not the same experiment as dietary zinc deficiency or zinc rescue.

nutrient_topic

L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine

plain_language

A metal-binding site can be a separate gate in nutrient recycling.

primary_references

Functional identification of APIP as human mtnB, a key enzyme in the methionine salvage pathway. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23285211/ · DOI 10.1371/journal.pone.0052877

trigger_kind

machinery_impairment Imported condition classification; unverified.

L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 316–322

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human APIP mutant-function study. · source_derived_draft · unverified_draft

## methionine-apip-zinc-site A metal-binding site can be a separate gate in nutrient recycling. Mutation of the predicted zinc-binding site abolished APIP salvage function, whereas three tested potential phosphorylation-site mutations did not. Model: Human APIP mutant-function study. Limitations: Mutating a metal-binding site is not the same experiment as dietary zinc deficiency or zinc rescue. Evidence access: Primary abstract Functional identification of APIP as human mtnB, a key enzyme in the methionine salvage pathway. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23285211/ · DOI 10.1371/journal.pone.0052877

evidence_span

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experimental_model

Refinement of the 2 angstrom crystal structure of copper, zinc superoxide dismutase with molecular surface analysis

exposure

Structural and mechanistic analysis of the active site

limitations

Structural chemistry. It explains why the enzyme needs its metals; it is not a statement about dietary copper or zinc.

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

Bovine enzyme structure

plain_language

The copper atom itself is what takes and gives back the electron.

primary_references

[hbot-p6316150] Structure and mechanism of copper, zinc superoxide dismutase. (1983). https://pubmed.ncbi.nlm.nih.gov/6316150/ DOI: 10.1038/306284a0

tissue_or_cell_type

Purified enzyme

Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 491–502

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Refinement of the 2 angstrom crystal structure of copper, zinc superoxide dismutase with molecular surface analysis · source_derived_draft · unverified_draft

### hbot-sod1-copper-mechanism Copper, zinc superoxide dismutase catalyses the two-step dismutation of superoxide to molecular oxygen and hydrogen peroxide through alternate reduction and oxidation of the active-site copper, with a single complementary binding position for superoxide at the Cu(II) and the activity-important Arg141. 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 copper atom itself is what takes and gives back the electron. organism: Bovine enzyme structure tissue_or_cell_type: Purified enzyme experimental_model: Refinement of the 2 angstrom crystal structure of copper, zinc superoxide dismutase with molecular surface analysis limitations: Structural chemistry. It explains why the enzyme needs its metals; it is not a statement about dietary copper or zinc. exposure: Structural and mechanistic analysis of the active site evidence_span: {"source_cache": "artifacts/hbot-research/6316150.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dc20323f9774c6c743e01f8bdbeedbc42b0ddac982f1e17d53a9591b87bf5379", "start_char": 0, "end_char": 867, "text_sha256": "dc20323f9774c6c743e01f8bdbeedbc42b0ddac982f1e17d53a9591b87bf5379"} [hbot-p6316150] Structure and mechanism of copper, zinc superoxide dismutase. (1983). https://pubmed.ncbi.nlm.nih.gov/6316150/ DOI: 10.1038/306284a0

evidence_span

{"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"}

experimental_model

Double-blind randomized placebo-controlled trial; 32 adults

exposure

24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo

limitations

Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Human with metabolic syndrome

plain_language

An inflammation marker changed even though the main metabolic measures did not.

primary_references

[chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022

tissue_or_cell_type

Metabolic-risk endpoints and CRP

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 640–651

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial; 32 adults · source_derived_draft · unverified_draft

### chromium-triple-mineral-crp The three-mineral regimen reduced serum CRP relative to placebo despite the lack of improvement in the measured metabolic-risk components. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammation marker changed even though the main metabolic measures did not. organism: Human with metabolic syndrome tissue_or_cell_type: Metabolic-risk endpoints and CRP experimental_model: Double-blind randomized placebo-controlled trial; 32 adults limitations: Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints. exposure: 24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo evidence_span: {"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"} [chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022

evidence_span

{"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"}

experimental_model

Double-blind randomized placebo-controlled trial; 32 adults

exposure

24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo

limitations

Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Human with metabolic syndrome

plain_language

Adding three minerals did not consistently improve the metabolic endpoints in this small trial.

primary_references

[chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022

tissue_or_cell_type

Circulating glucose; the paper describes serum glucose rather than a tissue-specific transport endpoint

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 627–638

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized placebo-controlled trial; 32 adults · source_derived_draft · unverified_draft

### chromium-triple-mineral-glycemia-null The zinc-magnesium-chromium regimen did not significantly improve measured metabolic-syndrome risk components, including serum glucose, relative to placebo. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding three minerals did not consistently improve the metabolic endpoints in this small trial. organism: Human with metabolic syndrome tissue_or_cell_type: Circulating glucose; the paper describes serum glucose rather than a tissue-specific transport endpoint experimental_model: Double-blind randomized placebo-controlled trial; 32 adults limitations: Only the three-mineral combination was tested; individual effects and synergy cannot be separated. Small sample and multiple endpoints. exposure: 24 weeks: 300 mg magnesium, 600 µg chromium and 36 mg zinc daily versus placebo evidence_span: {"source_cache": "artifacts/chromium-research/29773176.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067", "start_char": 0, "end_char": 1208, "text_sha256": "6107419f3b2f125a5a9971f56f24c1bd454a97512ef432f154c79d26b85c1067"} [chromium-p29773176] Effects of zinc, magnesium, and chromium supplementation on cardiometabolic risk in adults with metabolic syndrome: A double-blind, placebo-controlled randomised trial. (2018). https://pubmed.ncbi.nlm.nih.gov/29773176/ DOI: 10.1016/j.jtemb.2018.03.022

evidence_span

{"source_cache": "artifacts/curcumin-research/24634837.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7", "start_char": 0, "end_char": 1451, "text_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7"}

experimental_model

Six-month feeding comparison in C57BL/6J mice

exposure

Diet containing 0.2% curcumin versus unsupplemented diet

limitations

Long-term mouse findings cannot be equated with acute human supplementation. Expression changes may be adaptive responses, not direct target binding.

nutrient_topic

Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin

organism

Mus musculus

plain_language

This did not behave as indiscriminate stripping of every mineral.

primary_references

[curcumin-p24634837] Curcumin may impair iron status when fed to mice for six months. (2014). https://pubmed.ncbi.nlm.nih.gov/24634837/ DOI: 10.1016/j.redox.2014.01.018

tissue_or_cell_type

Liver and spleen

Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 710–721

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month feeding comparison in C57BL/6J mice · source_derived_draft · unverified_draft

### curcumin-mouse-zinc-null The study did not find reduced liver zinc stores. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This did not behave as indiscriminate stripping of every mineral. organism: Mus musculus tissue_or_cell_type: Liver and spleen experimental_model: Six-month feeding comparison in C57BL/6J mice limitations: Long-term mouse findings cannot be equated with acute human supplementation. Expression changes may be adaptive responses, not direct target binding. exposure: Diet containing 0.2% curcumin versus unsupplemented diet evidence_span: {"source_cache": "artifacts/curcumin-research/24634837.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7", "start_char": 0, "end_char": 1451, "text_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7"} [curcumin-p24634837] Curcumin may impair iron status when fed to mice for six months. (2014). https://pubmed.ncbi.nlm.nih.gov/24634837/ DOI: 10.1016/j.redox.2014.01.018

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Zinc (prior_exposure); Blood leukocyte count (increased_endpoint); Serum ceruloplasmin concentration (responsive_marker)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487}

experimental_model

Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy

exposure

Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered.

limitations

Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Copper replacement improved the reported blood-cell abnormalities.

primary_references

[zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019

tissue_or_cell_type

Blood copper and hematology

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1422–1435

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy · source_derived_draft · unverified_draft

### zn-clin-copper-response Copper administration increased erythrocyte size and leukocyte counts in the reported index patient; the authors also reported correction of hypoceruloplasminemia in additional zinc-treated patients. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper replacement improved the reported blood-cell abnormalities. organism: Homo sapiens tissue_or_cell_type: Blood copper and hematology experimental_model: Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy limitations: Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio. exposure: Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered. cross_nutrient: Zinc (prior_exposure); Blood leukocyte count (increased_endpoint); Serum ceruloplasmin concentration (responsive_marker) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487} [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019

absolute_absorption

Corresponding absolute absorption: 3.8±0.3, 3.0±0.3, 4.5±0.3 and 3.2±0.3 mg zinc/day (mean±SE).

cross_nutrient

Calcium (dietary_context); Zinc (measured_nutrient)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/hunt2009.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "d912d9f2c0890cde2ae13e9de7f1202bf130e661e3f14e13483563f179319f85", "utf8_bytes": 1659}

experimental_model

Two-by-two one-day feeding and 65Zn tracer study in ten healthy women

exposure

Approximately 700 versus 1800 mg calcium/day, and 440 versus 1800 mg phytate/day in conventional menus.

limitations

Short controlled menus in ten women; null calcium effect does not cover every formulation, population or dose.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Phytate reduced zinc uptake in these menus, while extra calcium did not.

primary_references

[zn-clin-hunt2009] Dietary calcium does not exacerbate phytate inhibition of zinc absorption by women from conventional diets. (2009). https://pubmed.ncbi.nlm.nih.gov/19176739/ DOI: 10.3945/ajcn.2008.27175

tissue_or_cell_type

Intestinal absorption

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1271–1285

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two-by-two one-day feeding and 65Zn tracer study in ten healthy women · source_derived_draft · unverified_draft

### zn-clin-phytate-calcium Zinc absorption fractions were 32.8±2.3%, 26.9±2.4%, 39.4±2.4% and 26.2±2.3% (mean±SE) for moderate-Ca/low-phytate, moderate-Ca/high-phytate, high-Ca/low-phytate and high-Ca/high-phytate menus. Phytate reduced absorption; calcium did not significantly impair it. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phytate reduced zinc uptake in these menus, while extra calcium did not. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption experimental_model: Two-by-two one-day feeding and 65Zn tracer study in ten healthy women limitations: Short controlled menus in ten women; null calcium effect does not cover every formulation, population or dose. exposure: Approximately 700 versus 1800 mg calcium/day, and 440 versus 1800 mg phytate/day in conventional menus. cross_nutrient: Calcium (dietary_context); Zinc (measured_nutrient) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/hunt2009.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "d912d9f2c0890cde2ae13e9de7f1202bf130e661e3f14e13483563f179319f85", "utf8_bytes": 1659} absolute_absorption: Corresponding absolute absorption: 3.8±0.3, 3.0±0.3, 4.5±0.3 and 3.2±0.3 mg zinc/day (mean±SE). [zn-clin-hunt2009] Dietary calcium does not exacerbate phytate inhibition of zinc absorption by women from conventional diets. (2009). https://pubmed.ncbi.nlm.nih.gov/19176739/ DOI: 10.3945/ajcn.2008.27175

cross_nutrient

Calcium (retained_nutrient); Zinc (concurrently_measured_nutrient)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/hallberg2006.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "3a8556f5e4076009ed9adbf018205c8a3b2d0aaae43cccc866dc6be0271451d4", "utf8_bytes": 1603}

experimental_model

Human dual-radioisotope meal study: 40 subjects, 105 meals

exposure

Wheat-roll meals contained 3.1 mg zinc and 266 mg calcium; added sodium phytate supplied 0–250 mg phytate phosphorus.

limitations

Phytate-P mass is phosphorus mass, not total phytate mass. Seven-day calcium retention and zinc absorption are distinct endpoints; meal-specific significance levels are not universal thresholds.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

The same meal manipulation also reduced retained calcium.

primary_references

[zn-clin-hallberg2006] Absorption of zinc and retention of calcium: dose-dependent inhibition by phytate. (2006). https://pubmed.ncbi.nlm.nih.gov/16632176/ DOI: 10.1016/j.jtemb.2006.01.003

tissue_or_cell_type

Intestinal zinc absorption and whole-body calcium retention

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1302–1315

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human dual-radioisotope meal study: 40 subjects, 105 meals · source_derived_draft · unverified_draft

### zn-clin-phytate-calcium-retention At the same ascending phytate-P additions, seven-day calcium retention was 31%, 28%, 27%, 26%, 22%, 19%, 14% and 11%; reduction was significant from 100 mg phytate-P in this study. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same meal manipulation also reduced retained calcium. organism: Homo sapiens tissue_or_cell_type: Intestinal zinc absorption and whole-body calcium retention experimental_model: Human dual-radioisotope meal study: 40 subjects, 105 meals limitations: Phytate-P mass is phosphorus mass, not total phytate mass. Seven-day calcium retention and zinc absorption are distinct endpoints; meal-specific significance levels are not universal thresholds. exposure: Wheat-roll meals contained 3.1 mg zinc and 266 mg calcium; added sodium phytate supplied 0–250 mg phytate phosphorus. cross_nutrient: Calcium (retained_nutrient); Zinc (concurrently_measured_nutrient) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/hallberg2006.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "3a8556f5e4076009ed9adbf018205c8a3b2d0aaae43cccc866dc6be0271451d4", "utf8_bytes": 1603} [zn-clin-hallberg2006] Absorption of zinc and retention of calcium: dose-dependent inhibition by phytate. (2006). https://pubmed.ncbi.nlm.nih.gov/16632176/ DOI: 10.1016/j.jtemb.2006.01.003

cross_nutrient

Zinc (absorbed_nutrient); Calcium (meal_context)

evidence_location

Indexed primary abstract.

evidence_span

{"source_cache": "artifacts/zinc-clinical-sources/hallberg2006.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "3a8556f5e4076009ed9adbf018205c8a3b2d0aaae43cccc866dc6be0271451d4", "utf8_bytes": 1603}

experimental_model

Human dual-radioisotope meal study: 40 subjects, 105 meals

exposure

Wheat-roll meals contained 3.1 mg zinc and 266 mg calcium; added sodium phytate supplied 0–250 mg phytate phosphorus.

limitations

Phytate-P mass is phosphorus mass, not total phytate mass. Seven-day calcium retention and zinc absorption are distinct endpoints; meal-specific significance levels are not universal thresholds.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Homo sapiens

plain_language

Increasing phytate progressively reduced zinc uptake in the test meal.

primary_references

[zn-clin-hallberg2006] Absorption of zinc and retention of calcium: dose-dependent inhibition by phytate. (2006). https://pubmed.ncbi.nlm.nih.gov/16632176/ DOI: 10.1016/j.jtemb.2006.01.003

tissue_or_cell_type

Intestinal zinc absorption and whole-body calcium retention

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1287–1300

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human dual-radioisotope meal study: 40 subjects, 105 meals · source_derived_draft · unverified_draft

### zn-clin-phytate-gradient At added phytate-P levels of 0, 25, 50, 75, 100, 140, 175 and 250 mg, mean zinc absorption was 22%, 16%, 14%, 11%, 7%, 7%, 7% and 6%. Reductions were significant from 50 mg phytate-P in these meals. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing phytate progressively reduced zinc uptake in the test meal. organism: Homo sapiens tissue_or_cell_type: Intestinal zinc absorption and whole-body calcium retention experimental_model: Human dual-radioisotope meal study: 40 subjects, 105 meals limitations: Phytate-P mass is phosphorus mass, not total phytate mass. Seven-day calcium retention and zinc absorption are distinct endpoints; meal-specific significance levels are not universal thresholds. exposure: Wheat-roll meals contained 3.1 mg zinc and 266 mg calcium; added sodium phytate supplied 0–250 mg phytate phosphorus. cross_nutrient: Zinc (absorbed_nutrient); Calcium (meal_context) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/hallberg2006.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "3a8556f5e4076009ed9adbf018205c8a3b2d0aaae43cccc866dc6be0271451d4", "utf8_bytes": 1603} [zn-clin-hallberg2006] Absorption of zinc and retention of calcium: dose-dependent inhibition by phytate. (2006). https://pubmed.ncbi.nlm.nih.gov/16632176/ DOI: 10.1016/j.jtemb.2006.01.003

cross_nutrient

Zinc (affected_nutrient); Rat intestinal metallothioneins measured without isoform resolution (unchanged_association)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"}

experimental_model

Dietary radiotracer experiments in rats

exposure

High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements.

limitations

High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

Copper also affected zinc absorption, with a different response pattern.

primary_references

[zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

tissue_or_cell_type

Small intestine

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 929–941

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary radiotracer experiments in rats · source_derived_draft · unverified_draft

### zn-sig-copper-zinc-absorption Raising rat dietary copper from 3 to 24 mg/kg reduced 65Zn absorption by about 20%; further increases to 300 mg/kg did not add inhibition or change zinc association with intestinal metallothionein. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper also affected zinc absorption, with a different response pattern. organism: Rattus norvegicus tissue_or_cell_type: Small intestine experimental_model: Dietary radiotracer experiments in rats limitations: High animal dietary concentrations are not human intake thresholds. Copper displacement from metallothionein was the authors’ mechanistic interpretation. exposure: High dietary zinc or copper and reciprocal 64Cu/65Zn absorption measurements. cross_nutrient: Zinc (affected_nutrient); Rat intestinal metallothioneins measured without isoform resolution (unchanged_association) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/479878-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "643b0358984f3caac8a20e3202c14a073d11ff88758c7a9637b6f8523195658b"} [zn-sig-479878] Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. (1979). https://pubmed.ncbi.nlm.nih.gov/479878/ DOI: 10.1016/s0162-0134(00)80054-9

cross_nutrient

Zinc (affected_nutrient)

evidence_span

{"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"}

experimental_model

Isolated vascularly perfused intestine from diet-conditioned rats

exposure

Dietary copper/zinc variation for one week versus direct luminal-metal variation.

limitations

Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption.

nutrient_topic

Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc

organism

Rattus norvegicus

plain_language

Copper altered zinc movement through, as well as into, intestinal cells.

primary_references

[zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

tissue_or_cell_type

Small-intestinal mucosa and portal effluent

Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 971–983

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated vascularly perfused intestine from diet-conditioned rats · source_derived_draft · unverified_draft

### zn-sig-luminal-copper-zinc High luminal copper increased mucosal zinc accumulation while reducing zinc transfer to portal effluent at the highest luminal zinc concentration. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper altered zinc movement through, as well as into, intestinal cells. organism: Rattus norvegicus tissue_or_cell_type: Small-intestinal mucosa and portal effluent experimental_model: Isolated vascularly perfused intestine from diet-conditioned rats limitations: Ex-vivo perfusion and extreme luminal exposure differ from whole-animal feeding; increased metallothionein-bound copper alone did not prove reduced net absorption. exposure: Dietary copper/zinc variation for one week versus direct luminal-metal variation. cross_nutrient: Zinc (affected_nutrient) evidence_span: {"source_cache": "artifacts/zinc-signaling-sources/3968585-abstract.txt", "locator": "Primary indexed abstract", "file_sha256": "ca588cec5326d23dd5f8c9b409ea66fc415043b95af456399e495b8131c8f6ed"} [zn-sig-3968585] Copper and zinc absorption in the rat: mechanism of mutual antagonism. (1985). https://pubmed.ncbi.nlm.nih.gov/3968585/ DOI: 10.1093/jn/115.2.159

evidence_span

{"source_cache": "artifacts/boron-research/7889890.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "73e5c915a0c7a8fa107ff62480430e94c1cf5c40648f37e08d0266394b05b70a", "start_char": 0, "end_char": 1729, "text_sha256": "73e5c915a0c7a8fa107ff62480430e94c1cf5c40648f37e08d0266394b05b70a"}

experimental_model

High-dose rat toxicity experiments with supporting cell assays

exposure

High boric-acid exposure; testis boron approximately 1–2 mM

limitations

High-exposure animal toxicity does not specify a human dietary threshold. The indexed abstract is truncated; no unreported plasminogen-activator or cAMP result is inferred.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Rat

plain_language

Mineral changes appeared too late to explain the start of the injury in this experiment.

primary_references

[boron-p7889890] Mechanism of the testicular toxicity of boric acid in rats: in vivo and in vitro studies. (1994). https://pubmed.ncbi.nlm.nih.gov/7889890/ DOI: 10.1289/ehp.94102s799

tissue_or_cell_type

Testis, brain, tissue flavins and isolated Leydig cells

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 1171–1182

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-dose rat toxicity experiments with supporting cell assays · source_derived_draft · unverified_draft

### boron-rat-testis-minerals-not-upstream Changes in testicular calcium, phosphorus and zinc did not precede atrophy in the rat boric-acid study, arguing against those measured changes as the initiating mechanism. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mineral changes appeared too late to explain the start of the injury in this experiment. organism: Rat tissue_or_cell_type: Testis, brain, tissue flavins and isolated Leydig cells experimental_model: High-dose rat toxicity experiments with supporting cell assays limitations: High-exposure animal toxicity does not specify a human dietary threshold. The indexed abstract is truncated; no unreported plasminogen-activator or cAMP result is inferred. exposure: High boric-acid exposure; testis boron approximately 1–2 mM evidence_span: {"source_cache": "artifacts/boron-research/7889890.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "73e5c915a0c7a8fa107ff62480430e94c1cf5c40648f37e08d0266394b05b70a", "start_char": 0, "end_char": 1729, "text_sha256": "73e5c915a0c7a8fa107ff62480430e94c1cf5c40648f37e08d0266394b05b70a"} [boron-p7889890] Mechanism of the testicular toxicity of boric acid in rats: in vivo and in vitro studies. (1994). https://pubmed.ncbi.nlm.nih.gov/7889890/ DOI: 10.1289/ehp.94102s799

evidence_span

{"source_cache": "artifacts/cold-research/10396606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fdd2deec82fad8f9e148848c443d5b173ec42c0e07d9045c59773f7109883a7b", "start_char": 0, "end_char": 1139, "text_sha256": "fdd2deec82fad8f9e148848c443d5b173ec42c0e07d9045c59773f7109883a7b"}

experimental_model

Winter swimmers compared with people who had never taken part, sampled for erythrocyte and plasma antioxidants

exposure

Habitual ice bathing

limitations

A cross-sectional comparison, so self-selection cannot be excluded. The authors frame it as adaptation to repeated oxidative stress.

nutrient_topic

Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion

organism

Human

plain_language

People who swim in ice water carry more antioxidant defence at rest.

primary_references

[cold-p10396606] Improved antioxidative protection in winter swimmers. (1999). https://pubmed.ncbi.nlm.nih.gov/10396606/ DOI: 10.1093/qjmed/92.4.193

tissue_or_cell_type

Erythrocytes and plasma

Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 689–700

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Winter swimmers compared with people who had never taken part, sampled for erythrocyte and plasma antioxidants · source_derived_draft · unverified_draft

### cold-winter-swimmer-antioxidants Baseline reduced glutathione concentration and erythrocyte superoxide dismutase and catalase activities were higher in winter swimmers than in controls, which the authors interpret as an adaptive response to repeated oxidative stress and postulate as a mechanism of increased tolerance to environmental stress. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: People who swim in ice water carry more antioxidant defence at rest. organism: Human tissue_or_cell_type: Erythrocytes and plasma experimental_model: Winter swimmers compared with people who had never taken part, sampled for erythrocyte and plasma antioxidants limitations: A cross-sectional comparison, so self-selection cannot be excluded. The authors frame it as adaptation to repeated oxidative stress. exposure: Habitual ice bathing evidence_span: {"source_cache": "artifacts/cold-research/10396606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fdd2deec82fad8f9e148848c443d5b173ec42c0e07d9045c59773f7109883a7b", "start_char": 0, "end_char": 1139, "text_sha256": "fdd2deec82fad8f9e148848c443d5b173ec42c0e07d9045c59773f7109883a7b"} [cold-p10396606] Improved antioxidative protection in winter swimmers. (1999). https://pubmed.ncbi.nlm.nih.gov/10396606/ DOI: 10.1093/qjmed/92.4.193

availability_state

biomarker_context Imported condition classification; unverified.

cross_nutrient

Zinc (affected_nutrient); Manganese (target_of_treatment)

evidence_span

{"source_cache": "artifacts/manganese-clinical-sources/stamelou2012.txt", "locator": "Clinical description; zinc fell during chelation", "file_sha256": "5d86a26fe564508fb382d1c8df61f531bfbaf06b69e2078b0999e3a3129555f6", "start_char": 9745, "end_char": 9841, "text_sha256": "7ef45c204f1cf372e58dcedb502d4047ace972fd9321bd2af7ccbda75d349439", "text_characters": 96}

experimental_model

Ten-year longitudinal report of one SLC30A10 patient

exposure

Calcium disodium edetate chelation; subsequent increase in chelation frequency and addition of oral ferrous fumarate.

limitations

Repeated observations in one previously described patient. Combined treatment changes prevent attribution of later benefit to iron alone; disease-specific treatment is not routine nutrient replacement.

nutrient_topic

Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese

organism

Homo sapiens

plain_language

Treatment aimed at manganese also lowered another essential mineral.

primary_references

[mn-clin-stamelou2012] Dystonia with brain manganese accumulation resulting from SLC30A10 mutations: a new treatable disorder. (2012). https://pubmed.ncbi.nlm.nih.gov/22926781/ DOI: 10.1002/mds.25138

tissue_or_cell_type

Urine, blood, brain MRI and motor function

trigger_kind

biomarker_context Imported condition classification; unverified.

Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1300–1312

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-year longitudinal report of one SLC30A10 patient · source_derived_draft · unverified_draft

### mn-clin-chelation-zinc-loss Zinc concentration fell during chelation and zinc sulfate was added. Condition category: biomarker_context nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Treatment aimed at manganese also lowered another essential mineral. organism: Homo sapiens tissue_or_cell_type: Urine, blood, brain MRI and motor function experimental_model: Ten-year longitudinal report of one SLC30A10 patient limitations: Repeated observations in one previously described patient. Combined treatment changes prevent attribution of later benefit to iron alone; disease-specific treatment is not routine nutrient replacement. exposure: Calcium disodium edetate chelation; subsequent increase in chelation frequency and addition of oral ferrous fumarate. cross_nutrient: Zinc (affected_nutrient); Manganese (target_of_treatment) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/stamelou2012.txt", "locator": "Clinical description; zinc fell during chelation", "file_sha256": "5d86a26fe564508fb382d1c8df61f531bfbaf06b69e2078b0999e3a3129555f6", "start_char": 9745, "end_char": 9841, "text_sha256": "7ef45c204f1cf372e58dcedb502d4047ace972fd9321bd2af7ccbda75d349439", "text_characters": 96} [mn-clin-stamelou2012] Dystonia with brain manganese accumulation resulting from SLC30A10 mutations: a new treatable disorder. (2012). https://pubmed.ncbi.nlm.nih.gov/22926781/ DOI: 10.1002/mds.25138

evidence_span

{"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"}

experimental_model

AREDS2 phase 3 factorial randomized trial

exposure

Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years

limitations

Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 .

nutrient_topic

Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein

organism

4203 adults aged 50–85 at elevated AMD progression risk

plain_language

Adding the pair did not meet the primary statistical threshold.

primary_references

[lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997

tissue_or_cell_type

Eyes with large drusen and/or fellow-eye advanced AMD

Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 723–734

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AREDS2 phase 3 factorial randomized trial · source_derived_draft · unverified_draft

### lutein-areds-primary-null Primary L+Z versus placebo comparison gave HR 0.90 (98.7% CI 0.76–1.07; P=0.12). Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding the pair did not meet the primary statistical threshold. organism: 4203 adults aged 50–85 at elevated AMD progression risk tissue_or_cell_type: Eyes with large drusen and/or fellow-eye advanced AMD experimental_model: AREDS2 phase 3 factorial randomized trial limitations: Combination and background treatment prevent attribution to lutein alone; primary contrast differs from replacement and main-effects analyses. Published correction 10.1001/jama.2013.6403 changes the Table 3 lung-neoplasm row label and Table 4 lung-neoplasm entries. These records use the indexed abstract and do not reproduce the uncorrected Table 4. Correction: https://jamanetwork.com/journals/jama/fullarticle/1710434 . exposure: Lutein 10 mg + zeaxanthin 2 mg daily; background AREDS formula; median five years evidence_span: {"source_cache": "artifacts/lutein-research/23644932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f", "start_char": 0, "end_char": 3037, "text_sha256": "1bd379926e56d7243222c2ef69d6367b74aede2b02faabfb77fadcbadf95008f"} [lutein-p23644932] Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration: the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. (2013). https://pubmed.ncbi.nlm.nih.gov/23644932/ DOI: 10.1001/jama.2013.4997

evidence_span

{"source_cache": "artifacts/pectin-research/6307932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1", "start_char": 0, "end_char": 1593, "text_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1"}

experimental_model

Within-person ileostomy balance study; six participants

exposure

15 g/day citrus pectin on days 5-7 of a 10-day low-fiber feeding protocol

limitations

Ileal apparent absorption and output are not whole-body status or clinical deficiency; the colon was bypassed.

nutrient_topic

Pectin research collection; topical membership is not evidence of a direct dietary effect. · Pectin, structurally heterogeneous plant polysaccharides

organism

Homo sapiens

plain_language

An in-vitro zinc-binding result cannot simply be substituted for a human absorption result.

primary_references

[pectin-p6307932] The effect of citrus pectin on the absorption of nutrients in the small intestine. (1983). https://pubmed.ncbi.nlm.nih.gov/6307932/

tissue_or_cell_type

Small intestine; ileal effluent

Pectin: metabolism, signaling and nutrient connections (2026-09-17) · lines 620–631

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person ileostomy balance study; six participants · source_derived_draft · unverified_draft

### pectin-ileal-zinc-null Apparent zinc absorption was unchanged in this study. Condition category: normal nutrient_topic: Pectin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An in-vitro zinc-binding result cannot simply be substituted for a human absorption result. organism: Homo sapiens tissue_or_cell_type: Small intestine; ileal effluent experimental_model: Within-person ileostomy balance study; six participants limitations: Ileal apparent absorption and output are not whole-body status or clinical deficiency; the colon was bypassed. exposure: 15 g/day citrus pectin on days 5-7 of a 10-day low-fiber feeding protocol evidence_span: {"source_cache": "artifacts/pectin-research/6307932.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1", "start_char": 0, "end_char": 1593, "text_sha256": "fd45607a7ff1d1a20dd52d145134da591847919c3db47ef8a8cf5693fb9f80a1"} [pectin-p6307932] The effect of citrus pectin on the absorption of nutrients in the small intestine. (1983). https://pubmed.ncbi.nlm.nih.gov/6307932/

cross_nutrient

Iron/zinc -> retinoid transport markers.

experimental_model

Same factorial trial.

limitations

Measured biomarkers do not prove the molecular mechanism.

nutrient_topic

Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A

organism

Homo sapiens

plain_language

The two minerals did not produce identical carrier-protein responses.

primary_references

[va-munoz2000] Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers (2000). https://pubmed.ncbi.nlm.nih.gov/10702174/ DOI: 10.1093/ajcn/71.3.789

tissue_or_cell_type

Plasma

Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1495–1505

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same factorial trial. · source_derived_draft · unverified_draft

### va-iron-improves-retinol-marker Iron increased plasma retinol, RBP and transthyretin; the combined iron/zinc arm increased retinol without significant carrier-protein increases. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two minerals did not produce identical carrier-protein responses. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Same factorial trial. limitations: Measured biomarkers do not prove the molecular mechanism. cross_nutrient: Iron/zinc -> retinoid transport markers. [va-munoz2000] Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers (2000). https://pubmed.ncbi.nlm.nih.gov/10702174/ DOI: 10.1093/ajcn/71.3.789

cross_nutrient

Zinc-folate: molecular catalytic-site dependency; dietary zinc deficiency was not tested.

experimental_model

Recombinant human GCPII crystallography

exposure

Glutamate, phosphate and inhibitor-bound structures

limitations

Structural cofactor evidence does not establish zinc intake thresholds.

nutrient_topic

Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)

organism

Homo sapiens

plain_language

The folate-processing enzyme contains a two-zinc catalytic site.

primary_references

[mesters2006] Structure of glutamate carboxypeptidase II, a drug target in neuronal damage and prostate cancer (2006). https://pubmed.ncbi.nlm.nih.gov/16467855/ DOI: 10.1038/sj.emboj.7600969

tissue_or_cell_type

Purified recombinant protein

Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 118–129

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human GCPII crystallography · source_derived_draft · unverified_draft

### folate-gcpii-zinc-catalytic-center Human GCPII crystal structures resolved two zinc ions at the catalytic center, bridged by water or hydroxide and Asp387. Condition category: normal nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The folate-processing enzyme contains a two-zinc catalytic site. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein experimental_model: Recombinant human GCPII crystallography limitations: Structural cofactor evidence does not establish zinc intake thresholds. exposure: Glutamate, phosphate and inhibitor-bound structures cross_nutrient: Zinc-folate: molecular catalytic-site dependency; dietary zinc deficiency was not tested. [mesters2006] Structure of glutamate carboxypeptidase II, a drug target in neuronal damage and prostate cancer (2006). https://pubmed.ncbi.nlm.nih.gov/16467855/ DOI: 10.1038/sj.emboj.7600969

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/alcohol-research/20167873.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e", "start_char": 0, "end_char": 1542, "text_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e"}

experimental_model

Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation

exposure

Four weeks of alcohol liquid diet; zinc deprivation in culture

limitations

The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Mouse

plain_language

Alcohol drains zinc from one specific stretch of gut, and that is exactly where it leaks.

primary_references

[alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009

tissue_or_cell_type

Ileum and Caco-2 monolayers

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 761–772

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation · source_derived_draft · unverified_draft

### alcohol-alcohol-ileal-zinc Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species, and significantly increased permeability of the ileum without affecting the duodenum or jejunum. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Alcohol drains zinc from one specific stretch of gut, and that is exactly where it leaks. organism: Mouse tissue_or_cell_type: Ileum and Caco-2 monolayers experimental_model: Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation limitations: The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells. exposure: Four weeks of alcohol liquid diet; zinc deprivation in culture evidence_span: {"source_cache": "artifacts/alcohol-research/20167873.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e", "start_char": 0, "end_char": 1542, "text_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e"} [alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009

evidence_span

{"source_cache": "artifacts/alcohol-research/26585415.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c", "start_char": 0, "end_char": 1907, "text_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c"}

experimental_model

Rat model of alcoholic liver disease with mitochondrial respiratory chain assays

exposure

Chronic alcohol feeding with zinc status measured

limitations

Assigns the reactive oxygen species source to a respiratory chain defect and ties it to zinc. A rat model of the disease.

nutrient_topic

Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol

organism

Rat

plain_language

The damaged energy chain leaks reactive oxygen, and short zinc makes it worse.

primary_references

[alcohol-p26585415] Defect of mitochondrial respiratory chain is a mechanism of ROS overproduction in a rat model of alcoholic liver disease: role of zinc deficiency. (2016). https://pubmed.ncbi.nlm.nih.gov/26585415/ DOI: 10.1152/ajpgi.00270.2015

tissue_or_cell_type

Liver mitochondria

Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 514–525

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat model of alcoholic liver disease with mitochondrial respiratory chain assays · source_derived_draft · unverified_draft

### alcohol-mitochondrial-ros A defect of the mitochondrial respiratory chain was identified as a mechanism of reactive oxygen species overproduction in a rat model of alcoholic liver disease, with a role for zinc deficiency. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The damaged energy chain leaks reactive oxygen, and short zinc makes it worse. organism: Rat tissue_or_cell_type: Liver mitochondria experimental_model: Rat model of alcoholic liver disease with mitochondrial respiratory chain assays limitations: Assigns the reactive oxygen species source to a respiratory chain defect and ties it to zinc. A rat model of the disease. exposure: Chronic alcohol feeding with zinc status measured evidence_span: {"source_cache": "artifacts/alcohol-research/26585415.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c", "start_char": 0, "end_char": 1907, "text_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c"} [alcohol-p26585415] Defect of mitochondrial respiratory chain is a mechanism of ROS overproduction in a rat model of alcoholic liver disease: role of zinc deficiency. (2016). https://pubmed.ncbi.nlm.nih.gov/26585415/ DOI: 10.1152/ajpgi.00270.2015