Boric acid / orthoboric acid / B(OH)3

evidence_span

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experimental_model

Purified Aplysia cyclase kinetics and electrospray complex analysis

exposure

Noncompetitive inhibition Ki 40.5 ± 0.5 mM boric acid; cADPR-binding assay pH 10.3

limitations

The enzyme was Aplysia cyclase, not human CD38. Millimolar enzyme inhibition and alkaline binding data do not establish effects of ordinary dietary boron.

nutrient_topic

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

organism

Aplysia enzyme; cell-free chemistry

plain_language

High boric-acid concentrations slowed an enzyme that makes a calcium messenger; this was a sea-hare enzyme experiment.

primary_references

[boron-p16545389] Boric acid inhibits adenosine diphosphate-ribosyl cyclase non-competitively. (2006). https://pubmed.ncbi.nlm.nih.gov/16545389/ DOI: 10.1016/j.chroma.2006.02.066

tissue_or_cell_type

Purified enzyme and metabolites

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 157–168

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified Aplysia cyclase kinetics and electrospray complex analysis · source_derived_draft · unverified_draft

### boron-aplysia-cyclase-inhibition Boric acid inhibited purified Aplysia ADP-ribosyl cyclase noncompetitively with a reported Ki of 40.5 ± 0.5 mM. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: High boric-acid concentrations slowed an enzyme that makes a calcium messenger; this was a sea-hare enzyme experiment. organism: Aplysia enzyme; cell-free chemistry tissue_or_cell_type: Purified enzyme and metabolites experimental_model: Purified Aplysia cyclase kinetics and electrospray complex analysis limitations: The enzyme was Aplysia cyclase, not human CD38. Millimolar enzyme inhibition and alkaline binding data do not establish effects of ordinary dietary boron. exposure: Noncompetitive inhibition Ki 40.5 ± 0.5 mM boric acid; cADPR-binding assay pH 10.3 evidence_span: {"source_cache": "artifacts/boron-research/16545389.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655", "start_char": 0, "end_char": 724, "text_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655"} [boron-p16545389] Boric acid inhibits adenosine diphosphate-ribosyl cyclase non-competitively. (2006). https://pubmed.ncbi.nlm.nih.gov/16545389/ DOI: 10.1016/j.chroma.2006.02.066

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

A regulator of the cellular stress response increased.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 391–402

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-atf4-abundance Boric acid increased ATF4 protein at one hour in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A regulator of the cellular stress response increased. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

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experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

A separate regulator of the ER stress response increased.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 404–415

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-atf6-abundance Boric acid increased ATF6 protein at 30 minutes in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate regulator of the ER stress response increased. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

The cells increased an ER protein-folding helper.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 443–454

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-bip-expression Boric-acid treatment increased GRP78/BiP expression alongside the ATF6 response in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased an ER protein-folding helper. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

The cells increased another protein involved in ER folding and calcium handling.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 456–467

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-calreticulin-expression Boric-acid treatment increased calreticulin expression in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased another protein involved in ER folding and calcium handling. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}

experimental_model

Human prostate cancer cell culture and mass spectrometry

exposure

Boric acid 100–1,000 µM; methylboronic acid comparator

limitations

These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.

nutrient_topic

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

organism

Human DU-145 cells; cell-free complex analysis

plain_language

The cells increased CD38 protein; more protein does not by itself prove more enzyme activity.

primary_references

[boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

tissue_or_cell_type

Prostate cancer cells

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 287–298

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

### boron-cd38-expression CD38 protein abundance increased across 0–1,000 µM boric-acid exposure in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased CD38 protein; more protein does not by itself prove more enzyme activity. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Prostate cancer cells experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

evidence_span

{"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}

experimental_model

Calcium imaging and flow cytometry in three human prostate cell lines

exposure

Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour

limitations

RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.

nutrient_topic

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

organism

Human DU-145, LNCaP and PWR1E cells

plain_language

Different prostate cell types needed different concentrations for the measured response.

primary_references

[boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

tissue_or_cell_type

Cancer and non-tumor prostate cell cultures

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 352–363

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

### boron-cell-type-calcium-threshold Significant inhibition of caffeine-evoked calcium release required 20 µM boric acid in LNCaP cells and 150 µM in non-tumor PWR1E cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different prostate cell types needed different concentrations for the measured response. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Factorial boron/vitamin-D3 feeding experiment in chicks

exposure

26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg

limitations

Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans.

nutrient_topic

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

organism

Day-old cockerel chicks

plain_language

Some metabolic changes from inadequate vitamin D improved in this chick experiment.

primary_references

[boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

tissue_or_cell_type

Plasma metabolism and growth plates

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (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 · Factorial boron/vitamin-D3 feeding experiment in chicks · source_derived_draft · unverified_draft

### boron-chick-glucose Boron supplementation returned elevated plasma glucose concentrations in vitamin-D3-inadequate chicks toward those in vitamin-D3-adequate chicks. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some metabolic changes from inadequate vitamin D improved in this chick experiment. organism: Day-old cockerel chicks tissue_or_cell_type: Plasma metabolism and growth plates experimental_model: Factorial boron/vitamin-D3 feeding experiment in chicks limitations: Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans. exposure: 26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg evidence_span: {"source_cache": "artifacts/boron-research/8140930.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc", "start_char": 0, "end_char": 1621, "text_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc"} [boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

evidence_span

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experimental_model

Factorial boron/vitamin-D3 feeding experiment in chicks

exposure

26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg

limitations

Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans.

nutrient_topic

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

organism

Day-old cockerel chicks

plain_language

The developing growth plate appeared to mature differently; this is an animal histology finding.

primary_references

[boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

tissue_or_cell_type

Plasma metabolism and growth plates

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 872–883

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Factorial boron/vitamin-D3 feeding experiment in chicks · source_derived_draft · unverified_draft

### boron-chick-growth-plate Growth-plate histology suggested enhanced maturation with boron supplementation in the chick feeding experiment. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The developing growth plate appeared to mature differently; this is an animal histology finding. organism: Day-old cockerel chicks tissue_or_cell_type: Plasma metabolism and growth plates experimental_model: Factorial boron/vitamin-D3 feeding experiment in chicks limitations: Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans. exposure: 26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg evidence_span: {"source_cache": "artifacts/boron-research/8140930.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc", "start_char": 0, "end_char": 1621, "text_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc"} [boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

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experimental_model

Factorial boron/vitamin-D3 feeding experiment in chicks

exposure

26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg

limitations

Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans.

nutrient_topic

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

organism

Day-old cockerel chicks

plain_language

Some metabolic changes from inadequate vitamin D improved in this chick experiment.

primary_references

[boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

tissue_or_cell_type

Plasma metabolism and growth plates

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 859–870

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Factorial boron/vitamin-D3 feeding experiment in chicks · source_derived_draft · unverified_draft

### boron-chick-triglycerides Boron supplementation returned elevated plasma triglyceride concentrations in vitamin-D3-inadequate chicks toward those in vitamin-D3-adequate chicks. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some metabolic changes from inadequate vitamin D improved in this chick experiment. organism: Day-old cockerel chicks tissue_or_cell_type: Plasma metabolism and growth plates experimental_model: Factorial boron/vitamin-D3 feeding experiment in chicks limitations: Animal developmental experiment. It did not demonstrate direct CYP24A1 inhibition or that boron replaces vitamin D in humans. exposure: 26 days; basal boron ≤0.18 mg/kg with 0 or 1.4 mg/kg orthoboric acid supplement; vitamin D3 3.13 or 15.6 µg/kg evidence_span: {"source_cache": "artifacts/boron-research/8140930.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc", "start_char": 0, "end_char": 1621, "text_sha256": "6f8776234acbd0efd282761bbbcb0f51b39d8882c651b3f64686a890f646d4fc"} [boron-p8140930] Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick. (1994). https://pubmed.ncbi.nlm.nih.gov/8140930/ DOI: 10.1002/jbmr.5650090206

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

The stress response was selective; a signal linked to cell death decreased.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 482–493

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-chop-expression Boric-acid treatment decreased the pro-apoptotic CHOP/GADD153 response in DU-145 cells despite increasing several other ER-stress-associated genes. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The stress response was selective; a signal linked to cell death decreased. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

The amount of a translation-control protein increased; this measurement is distinct from its phosphorylation.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 378–389

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-eif2alpha-abundance Boric acid increased total eIF2α protein at 30 minutes in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The amount of a translation-control protein increased; this measurement is distinct from its phosphorylation. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}

experimental_model

Calcium imaging and flow cytometry in three human prostate cell lines

exposure

Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour

limitations

RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.

nutrient_topic

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

organism

Human DU-145, LNCaP and PWR1E cells

plain_language

Less calcium remained in the measured internal stores after exposure.

primary_references

[boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

tissue_or_cell_type

Cancer and non-tumor prostate cell cultures

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 339–350

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

### boron-er-calcium-storage Exposure to 50 µM boric acid for one hour reduced stored calcium by 32% in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less calcium remained in the measured internal stores after exposure. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

A feedback component of the stress response increased.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 417–428

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-gadd34-expression Boric-acid treatment increased GADD34 expression alongside the ATF4 response in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A feedback component of the stress response increased. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Human

plain_language

The cells increased instructions for GCLC; this does not measure the protein’s activity or a health benefit.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

DU-145 prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 560–571

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-gclc-transcription Boric acid increased GCLC mRNA at measured time points within 1–4 hours in human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased instructions for GCLC; this does not measure the protein’s activity or a health benefit. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

An additional ER protein-folding helper increased.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 469–480

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-grp94-expression Boric-acid treatment increased GRP94 expression in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: An additional ER protein-folding helper increased. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"}

experimental_model

Time-course immunoblotting and ER-stress gene expression

exposure

10 µM boric acid; early time points from 30 minutes

limitations

Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

A protein involved in handling ER stress increased; its name does not show that boron changes homocysteine metabolism.

primary_references

[boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 430–441

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Time-course immunoblotting and ER-stress gene expression · source_derived_draft · unverified_draft

### boron-herp-expression Boric-acid treatment increased HERP expression alongside the ATF4 response in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A protein involved in handling ER stress increased; its name does not show that boron changes homocysteine metabolism. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Time-course immunoblotting and ER-stress gene expression limitations: Expression changes do not establish direct molecular targets or clinical effects. Total eIF2α abundance is distinct from Ser51 phosphorylation. The study did not activate every ER-stress branch. exposure: 10 µM boric acid; early time points from 30 minutes evidence_span: {"source_cache": "artifacts/boron-research/27587023.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725", "start_char": 0, "end_char": 1886, "text_sha256": "421c3ea56e2b1058bb780928a63bb648246560a0ba3a070d82dc3fdd37ff0725"} [boron-p27587023] Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake. (2017). https://pubmed.ncbi.nlm.nih.gov/27587023/ DOI: 10.1007/s12011-016-0824-y

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Human

plain_language

The cells increased instructions for HMOX1; this does not measure the protein’s activity or a health benefit.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

DU-145 prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 534–545

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-hmox1-transcription Boric acid increased HMOX1 mRNA at measured time points within 1–4 hours in human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased instructions for HMOX1; this does not measure the protein’s activity or a health benefit. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Human

plain_language

An antioxidant-response regulator moved to the place where it can influence gene expression.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

DU-145 prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 521–532

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-human-nrf2-localization Nrf2 moved from the cytoplasm to the nucleus at 1.5–2 hours after boric-acid treatment of human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: An antioxidant-response regulator moved to the place where it can influence gene expression. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}

experimental_model

Human prostate cancer cell culture and mass spectrometry

exposure

Boric acid 100–1,000 µM; methylboronic acid comparator

limitations

These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.

nutrient_topic

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

organism

Human DU-145 cells; cell-free complex analysis

plain_language

At the tested concentrations, boric acid reduced several ways these cancer cells released stored calcium.

primary_references

[boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

tissue_or_cell_type

Prostate cancer cells

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 274–285

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

### boron-nad-calcium-response Boric acid partly inhibited NAD+-evoked calcium transients at 250 µM and completely at 1,000 µM in DU-145 cells; NADP+-evoked and mechanical responses were inhibited at 1,000 µM. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: At the tested concentrations, boric acid reduced several ways these cancer cells released stored calcium. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Prostate cancer cells experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Human

plain_language

The cells increased instructions for NQO1; this does not measure the protein’s activity or a health benefit.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

DU-145 prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 547–558

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-nqo1-transcription Boric acid increased NQO1 mRNA at measured time points within 1–4 hours in human DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased instructions for NQO1; this does not measure the protein’s activity or a health benefit. organism: Human tissue_or_cell_type: DU-145 prostate cancer cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/boron-research/6732506.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61", "start_char": 0, "end_char": 652, "text_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61"}

experimental_model

Single-dose intravenous pharmacokinetics in eight adult men

exposure

562–611 mg boric acid over 20 minutes; plasma followed three days and urine 120 hours

limitations

Historical intravenous experimental exposure is not an oral supplement regimen. These kinetics should not be generalized to kidney impairment or every exposure route.

nutrient_topic

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

organism

Human

plain_language

The measured blood level reflected elimination over roughly a day, with variation among participants.

primary_references

[boron-p6732506] Boric acid single dose pharmacokinetics after intravenous administration to man. (1984). https://pubmed.ncbi.nlm.nih.gov/6732506/ DOI: 10.1007/bf00316588

tissue_or_cell_type

Plasma and urine; six participants included in compartment fitting

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 1106–1117

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose intravenous pharmacokinetics in eight adult men · source_derived_draft · unverified_draft

### boron-plasma-kinetics The fitted terminal boric-acid half-life was 21.0 ± 4.9 hours and total clearance 54.6 ± 8.0 mL/min/1.73 m² in the intravenous study. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured blood level reflected elimination over roughly a day, with variation among participants. organism: Human tissue_or_cell_type: Plasma and urine; six participants included in compartment fitting experimental_model: Single-dose intravenous pharmacokinetics in eight adult men limitations: Historical intravenous experimental exposure is not an oral supplement regimen. These kinetics should not be generalized to kidney impairment or every exposure route. exposure: 562–611 mg boric acid over 20 minutes; plasma followed three days and urine 120 hours evidence_span: {"source_cache": "artifacts/boron-research/6732506.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61", "start_char": 0, "end_char": 652, "text_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61"} [boron-p6732506] Boric acid single dose pharmacokinetics after intravenous administration to man. (1984). https://pubmed.ncbi.nlm.nih.gov/6732506/ DOI: 10.1007/bf00316588

evidence_span

{"source_cache": "artifacts/boron-research/659962.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "903bb51f45f538c7ce8d0a73e5247e4619efb74ce4cd3fa8fc06f9bf108ba92f", "start_char": 0, "end_char": 696, "text_sha256": "903bb51f45f538c7ce8d0a73e5247e4619efb74ce4cd3fa8fc06f9bf108ba92f"}

experimental_model

Poison-control case series; 14 children and adults

exposure

Poisoning-related ingestion; most increased urinary riboflavin appeared in the first 24 hours

limitations

Uncontrolled case series, not ordinary dietary exposure. Increased excretion does not alone establish tissue deficiency or the responsible molecular transport mechanism.

nutrient_topic

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

organism

Human

plain_language

High boric-acid exposure was associated with loss of vitamin B2 into urine in this case series.

primary_references

[boron-p659962] Increased urinary riboflavin excretion resulting from boric acid ingestion. (1978). https://pubmed.ncbi.nlm.nih.gov/659962/

tissue_or_cell_type

Urine after boric-acid ingestion

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 937–948

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Poison-control case series; 14 children and adults · source_derived_draft · unverified_draft

### boron-poisoning-riboflavinuria Approximately two thirds of 14 patients evaluated after boric-acid ingestion had markedly increased urinary riboflavin excretion. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: High boric-acid exposure was associated with loss of vitamin B2 into urine in this case series. organism: Human tissue_or_cell_type: Urine after boric-acid ingestion experimental_model: Poison-control case series; 14 children and adults limitations: Uncontrolled case series, not ordinary dietary exposure. Increased excretion does not alone establish tissue deficiency or the responsible molecular transport mechanism. exposure: Poisoning-related ingestion; most increased urinary riboflavin appeared in the first 24 hours evidence_span: {"source_cache": "artifacts/boron-research/659962.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "903bb51f45f538c7ce8d0a73e5247e4619efb74ce4cd3fa8fc06f9bf108ba92f", "start_char": 0, "end_char": 696, "text_sha256": "903bb51f45f538c7ce8d0a73e5247e4619efb74ce4cd3fa8fc06f9bf108ba92f"} [boron-p659962] Increased urinary riboflavin excretion resulting from boric acid ingestion. (1978). https://pubmed.ncbi.nlm.nih.gov/659962/

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

At high exposures, the rat testis failed to release developing sperm normally.

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 1145–1156

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-spermiation-toxicity High-dose boric acid inhibited spermiation in adult rats, with lesions able to progress to testicular atrophy. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: At high exposures, the rat testis failed to release developing sperm normally. 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/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/boron-research/6732506.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61", "start_char": 0, "end_char": 652, "text_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61"}

experimental_model

Single-dose intravenous pharmacokinetics in eight adult men

exposure

562–611 mg boric acid over 20 minutes; plasma followed three days and urine 120 hours

limitations

Historical intravenous experimental exposure is not an oral supplement regimen. These kinetics should not be generalized to kidney impairment or every exposure route.

nutrient_topic

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

organism

Human

plain_language

The kidneys removed almost all of the administered amount over the collection period.

primary_references

[boron-p6732506] Boric acid single dose pharmacokinetics after intravenous administration to man. (1984). https://pubmed.ncbi.nlm.nih.gov/6732506/ DOI: 10.1007/bf00316588

tissue_or_cell_type

Plasma and urine; six participants included in compartment fitting

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 1093–1104

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-dose intravenous pharmacokinetics in eight adult men · source_derived_draft · unverified_draft

### boron-renal-elimination After intravenous boric acid, urinary recovery over 120 hours was 98.7 ± 9.1% of the dose. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys removed almost all of the administered amount over the collection period. organism: Human tissue_or_cell_type: Plasma and urine; six participants included in compartment fitting experimental_model: Single-dose intravenous pharmacokinetics in eight adult men limitations: Historical intravenous experimental exposure is not an oral supplement regimen. These kinetics should not be generalized to kidney impairment or every exposure route. exposure: 562–611 mg boric acid over 20 minutes; plasma followed three days and urine 120 hours evidence_span: {"source_cache": "artifacts/boron-research/6732506.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61", "start_char": 0, "end_char": 652, "text_sha256": "7deee2df94fd1ab9d173e7ddf97660bd8402d51bed8ac2bb8cac8810be66ca61"} [boron-p6732506] Boric acid single dose pharmacokinetics after intravenous administration to man. (1984). https://pubmed.ncbi.nlm.nih.gov/6732506/ DOI: 10.1007/bf00316588

evidence_span

{"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"}

experimental_model

Calcium imaging and flow cytometry in three human prostate cell lines

exposure

Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour

limitations

RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer.

nutrient_topic

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

organism

Human DU-145, LNCaP and PWR1E cells

plain_language

Boric acid changed release from a particular calcium store in these cells.

primary_references

[boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

tissue_or_cell_type

Cancer and non-tumor prostate cell cultures

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 326–337

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcium imaging and flow cytometry in three human prostate cell lines · source_derived_draft · unverified_draft

### boron-ryr-sensitive-calcium Boric acid reduced calcium release evoked by ryanodine-receptor agonists in DU-145 cells; cADPR inhibition was detected at 50 µM and responses to other agonists at different concentrations. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boric acid changed release from a particular calcium store in these cells. organism: Human DU-145, LNCaP and PWR1E cells tissue_or_cell_type: Cancer and non-tumor prostate cell cultures experimental_model: Calcium imaging and flow cytometry in three human prostate cell lines limitations: RyR-sensitive flux is not proof of direct binding to a particular RyR isoform. Cell-line exposure responses do not establish dietary prevention of prostate cancer. exposure: Boric acid 1–150 µM depending on agonist and cell line; DU-145 storage assay 50 µM for 1 hour evidence_span: {"source_cache": "artifacts/boron-research/19554099.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb", "start_char": 0, "end_char": 1809, "text_sha256": "17bd65bde36f54d1bb0688118212419b31643b9fc61323d12ef1ad6a78a173bb"} [boron-p19554099] Receptor activated Ca(2+) release is inhibited by boric acid in prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/19554099/ DOI: 10.1371/journal.pone.0006009

evidence_span

{"source_cache": "artifacts/boron-research/25425213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bd1560c24d673e3b1d1fc3d44f0c910ac981ffd2f53a3b90c6259f136c69fca", "start_char": 0, "end_char": 1068, "text_sha256": "5bd1560c24d673e3b1d1fc3d44f0c910ac981ffd2f53a3b90c6259f136c69fca"}

experimental_model

Human prostate cancer cell stress-response assays

exposure

Boric-acid exposure in the physiological-range conditions reported by the study

limitations

This study measured stress responses in a tumor cell line. Proposed consequences for bone differentiation or cancer risk were not tested clinical outcomes.

nutrient_topic

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

organism

Human DU-145 cells

plain_language

These cells reorganized parts of their protein-making machinery as a mild stress response.

primary_references

[boron-p25425213] Boric acid induces cytoplasmic stress granule formation, eIF2α phosphorylation, and ATF4 in prostate DU-145 cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25425213/ DOI: 10.1007/s10534-014-9809-5

tissue_or_cell_type

Prostate cancer cell culture

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 365–376

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell stress-response assays · source_derived_draft · unverified_draft

### boron-stress-granules Boric-acid treatment induced stress granules and mild activation of the eIF2α/ATF4 response in DU-145 cells. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: These cells reorganized parts of their protein-making machinery as a mild stress response. organism: Human DU-145 cells tissue_or_cell_type: Prostate cancer cell culture experimental_model: Human prostate cancer cell stress-response assays limitations: This study measured stress responses in a tumor cell line. Proposed consequences for bone differentiation or cancer risk were not tested clinical outcomes. exposure: Boric-acid exposure in the physiological-range conditions reported by the study evidence_span: {"source_cache": "artifacts/boron-research/25425213.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5bd1560c24d673e3b1d1fc3d44f0c910ac981ffd2f53a3b90c6259f136c69fca", "start_char": 0, "end_char": 1068, "text_sha256": "5bd1560c24d673e3b1d1fc3d44f0c910ac981ffd2f53a3b90c6259f136c69fca"} [boron-p25425213] Boric acid induces cytoplasmic stress granule formation, eIF2α phosphorylation, and ATF4 in prostate DU-145 cells. (2015). https://pubmed.ncbi.nlm.nih.gov/25425213/ DOI: 10.1007/s10534-014-9809-5

evidence_span

{"source_cache": "artifacts/boron-research/16545389.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655", "start_char": 0, "end_char": 724, "text_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655"}

experimental_model

Purified Aplysia cyclase kinetics and electrospray complex analysis

exposure

Noncompetitive inhibition Ki 40.5 ± 0.5 mM boric acid; cADPR-binding assay pH 10.3

limitations

The enzyme was Aplysia cyclase, not human CD38. Millimolar enzyme inhibition and alkaline binding data do not establish effects of ordinary dietary boron.

nutrient_topic

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

organism

Aplysia enzyme; cell-free chemistry

plain_language

Boron can complex the calcium messenger cADPR under the tested chemical conditions.

primary_references

[boron-p16545389] Boric acid inhibits adenosine diphosphate-ribosyl cyclase non-competitively. (2006). https://pubmed.ncbi.nlm.nih.gov/16545389/ DOI: 10.1016/j.chroma.2006.02.066

tissue_or_cell_type

Purified enzyme and metabolites

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 170–181

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified Aplysia cyclase kinetics and electrospray complex analysis · source_derived_draft · unverified_draft

### boron-cadpr-binding Boric acid bound cyclic ADP-ribose with an apparent association constant of 655 ± 99 L/mol in the electrospray assay at pH 10.3. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boron can complex the calcium messenger cADPR under the tested chemical conditions. organism: Aplysia enzyme; cell-free chemistry tissue_or_cell_type: Purified enzyme and metabolites experimental_model: Purified Aplysia cyclase kinetics and electrospray complex analysis limitations: The enzyme was Aplysia cyclase, not human CD38. Millimolar enzyme inhibition and alkaline binding data do not establish effects of ordinary dietary boron. exposure: Noncompetitive inhibition Ki 40.5 ± 0.5 mM boric acid; cADPR-binding assay pH 10.3 evidence_span: {"source_cache": "artifacts/boron-research/16545389.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655", "start_char": 0, "end_char": 724, "text_sha256": "720b1c99bd2628157e48db8085947552afc30029faeb65fb9235541b95c4b655"} [boron-p16545389] Boric acid inhibits adenosine diphosphate-ribosyl cyclase non-competitively. (2006). https://pubmed.ncbi.nlm.nih.gov/16545389/ DOI: 10.1016/j.chroma.2006.02.066

evidence_span

{"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}

experimental_model

Human prostate cancer cell culture and mass spectrometry

exposure

Boric acid 100–1,000 µM; methylboronic acid comparator

limitations

These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.

nutrient_topic

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

organism

Human DU-145 cells; cell-free complex analysis

plain_language

The study found a chemical interaction with cADPR, while its cellular role still requires separate evidence.

primary_references

[boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

tissue_or_cell_type

Cell-free mass-spectrometry assay associated with the cell study

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 313–324

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

### boron-cadpr-complex-cell-study Mass spectrometry detected boric-acid adducts of cyclic ADP-ribose in the study of DU-145 calcium signaling. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study found a chemical interaction with cADPR, while its cellular role still requires separate evidence. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Cell-free mass-spectrometry assay associated with the cell study experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

evidence_span

{"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"}

experimental_model

Human prostate cancer cell culture and mass spectrometry

exposure

Boric acid 100–1,000 µM; methylboronic acid comparator

limitations

These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding.

nutrient_topic

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

organism

Human DU-145 cells; cell-free complex analysis

plain_language

Boron can attach to another calcium-signaling molecule, NAADP, in the chemical assay.

primary_references

[boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

tissue_or_cell_type

Cell-free mass-spectrometry assay associated with the cell study

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 300–311

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human prostate cancer cell culture and mass spectrometry · source_derived_draft · unverified_draft

### boron-naadp-complex Mass spectrometry detected boric-acid adducts of NAADP in the study of DU-145 calcium signaling. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boron can attach to another calcium-signaling molecule, NAADP, in the chemical assay. organism: Human DU-145 cells; cell-free complex analysis tissue_or_cell_type: Cell-free mass-spectrometry assay associated with the cell study experimental_model: Human prostate cancer cell culture and mass spectrometry limitations: These are cell-culture exposures, including concentrations far above usual circulating levels. Adduct detection and calcium responses do not prove cancer prevention or direct channel binding. exposure: Boric acid 100–1,000 µM; methylboronic acid comparator evidence_span: {"source_cache": "artifacts/boron-research/18516691.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206", "start_char": 0, "end_char": 1733, "text_sha256": "5fc4f02e11634c2a2d111a99ee4c6175fe8839a8f28152b656b3c29be6745206"} [boron-p18516691] Boric acid inhibits stored Ca2+ release in DU-145 prostate cancer cells. (2009). https://pubmed.ncbi.nlm.nih.gov/18516691/ DOI: 10.1007/s10565-008-9085-7

evidence_span

{"source_cache": "artifacts/boron-research/12827632.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6", "start_char": 0, "end_char": 1255, "text_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6"}

experimental_model

Electrospray mass spectrometry and boron-11 NMR

exposure

NAD+/NADH with boric acid or borate across pH conditions; complexes detected at 50 µM each at pH 7

limitations

Chemical structure experiments do not establish cellular concentrations or physiological consequences.

nutrient_topic

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

organism

Cell-free chemistry

plain_language

Boron attaches to the sugar portion of NAD+ in these experiments.

primary_references

[boron-p12827632] Esterification of borate with NAD+ and NADH as studied by electrospray ionization mass spectrometry and 11B NMR spectroscopy. (2003). https://pubmed.ncbi.nlm.nih.gov/12827632/ DOI: 10.1002/jms.476

tissue_or_cell_type

Purified nucleotide solutions

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (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 · Electrospray mass spectrometry and boron-11 NMR · source_derived_draft · unverified_draft

### boron-nad-adduct-structure NAD+ formed monoester, diester and diborate adducts through ribose cis-2,3-diol groups rather than phosphate hydroxyls; the 1:1 monoester localized to the adenosine ribose. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Boron attaches to the sugar portion of NAD+ in these experiments. organism: Cell-free chemistry tissue_or_cell_type: Purified nucleotide solutions experimental_model: Electrospray mass spectrometry and boron-11 NMR limitations: Chemical structure experiments do not establish cellular concentrations or physiological consequences. exposure: NAD+/NADH with boric acid or borate across pH conditions; complexes detected at 50 µM each at pH 7 evidence_span: {"source_cache": "artifacts/boron-research/12827632.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6", "start_char": 0, "end_char": 1255, "text_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6"} [boron-p12827632] Esterification of borate with NAD+ and NADH as studied by electrospray ionization mass spectrometry and 11B NMR spectroscopy. (2003). https://pubmed.ncbi.nlm.nih.gov/12827632/ DOI: 10.1002/jms.476

evidence_span

{"source_cache": "artifacts/boron-research/15282753.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9385dca91d3dc7bb5a3d2a9c71a8e4c4ec0af136a15de2ea9536365a048d8057", "start_char": 0, "end_char": 1378, "text_sha256": "9385dca91d3dc7bb5a3d2a9c71a8e4c4ec0af136a15de2ea9536365a048d8057"}

experimental_model

Electrospray mass spectrometry comparing nucleotide binding

exposure

100 µM nucleotide and 500 µM boric acid in WAT solvent at pH 10.3; separate pH 7.4 ammonium bicarbonate condition

limitations

Relative ion signals and assay-specific rankings cannot be treated as universal binding constants or in-vivo metabolic effects.

nutrient_topic

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

organism

Cell-free chemistry

plain_language

Added phosphate groups and the test solution change the observed binding pattern.

primary_references

[boron-p15282753] Borate-nucleotide complex formation depends on charge and phosphorylation state. (2004). https://pubmed.ncbi.nlm.nih.gov/15282753/ DOI: 10.1002/jms.645

tissue_or_cell_type

Purified nucleotide solutions

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 144–155

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrospray mass spectrometry comparing nucleotide binding · source_derived_draft · unverified_draft

### boron-nad-phosphate-context The reported boron-binding order was NAD+ > NADH > NADP+ > NADPH at pH 10.3; only the NAD+ complex was observed in the separate pH 7.4 ammonium-bicarbonate condition. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Added phosphate groups and the test solution change the observed binding pattern. organism: Cell-free chemistry tissue_or_cell_type: Purified nucleotide solutions experimental_model: Electrospray mass spectrometry comparing nucleotide binding limitations: Relative ion signals and assay-specific rankings cannot be treated as universal binding constants or in-vivo metabolic effects. exposure: 100 µM nucleotide and 500 µM boric acid in WAT solvent at pH 10.3; separate pH 7.4 ammonium bicarbonate condition evidence_span: {"source_cache": "artifacts/boron-research/15282753.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9385dca91d3dc7bb5a3d2a9c71a8e4c4ec0af136a15de2ea9536365a048d8057", "start_char": 0, "end_char": 1378, "text_sha256": "9385dca91d3dc7bb5a3d2a9c71a8e4c4ec0af136a15de2ea9536365a048d8057"} [boron-p15282753] Borate-nucleotide complex formation depends on charge and phosphorylation state. (2004). https://pubmed.ncbi.nlm.nih.gov/15282753/ DOI: 10.1002/jms.645

evidence_span

{"source_cache": "artifacts/boron-research/12827632.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6", "start_char": 0, "end_char": 1255, "text_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6"}

experimental_model

Electrospray mass spectrometry and boron-11 NMR

exposure

NAD+/NADH with boric acid or borate across pH conditions; complexes detected at 50 µM each at pH 7

limitations

Chemical structure experiments do not establish cellular concentrations or physiological consequences.

nutrient_topic

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

organism

Cell-free chemistry

plain_language

Oxidized and reduced NAD do not necessarily make the same boron complexes.

primary_references

[boron-p12827632] Esterification of borate with NAD+ and NADH as studied by electrospray ionization mass spectrometry and 11B NMR spectroscopy. (2003). https://pubmed.ncbi.nlm.nih.gov/12827632/ DOI: 10.1002/jms.476

tissue_or_cell_type

Purified nucleotide solutions

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 131–142

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrospray mass spectrometry and boron-11 NMR · source_derived_draft · unverified_draft

### boron-nadh-adduct-structure NADH formed a monoester boron adduct in the analyzed solutions, whereas the additional diester and diborate forms observed for NAD+ were not detected for NADH. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Oxidized and reduced NAD do not necessarily make the same boron complexes. organism: Cell-free chemistry tissue_or_cell_type: Purified nucleotide solutions experimental_model: Electrospray mass spectrometry and boron-11 NMR limitations: Chemical structure experiments do not establish cellular concentrations or physiological consequences. exposure: NAD+/NADH with boric acid or borate across pH conditions; complexes detected at 50 µM each at pH 7 evidence_span: {"source_cache": "artifacts/boron-research/12827632.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6", "start_char": 0, "end_char": 1255, "text_sha256": "a7c91724a5710f61e1907669a1137b421e1e13117ae707e567bd16ca0eea9ed6"} [boron-p12827632] Esterification of borate with NAD+ and NADH as studied by electrospray ionization mass spectrometry and 11B NMR spectroscopy. (2003). https://pubmed.ncbi.nlm.nih.gov/12827632/ DOI: 10.1002/jms.476

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Mouse embryonic fibroblasts and human DU-145 cells

plain_language

Removing PERK blocked this step of the boric-acid response.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

Cell culture

trigger_kind

machinery_impairment Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 495–506

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-perk-eif2alpha-dependence Boric acid induced eIF2α Ser51 phosphorylation in wild-type mouse fibroblasts at one hour, but not in Perk-null cells tested for up to six hours. Condition category: machinery_impairment nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing PERK blocked this step of the boric-acid response. organism: Mouse embryonic fibroblasts and human DU-145 cells tissue_or_cell_type: Cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}

experimental_model

PERK knockout comparison, immunofluorescence and quantitative PCR

exposure

10 µM boric acid; 1–6 hour comparisons

limitations

Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.

nutrient_topic

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

organism

Mouse embryonic fibroblasts and human DU-145 cells

plain_language

PERK was also needed for the measured movement of Nrf2 into the nucleus.

primary_references

[boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

tissue_or_cell_type

Cell culture

trigger_kind

machinery_impairment Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 508–519

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft

### boron-perk-nrf2-dependence Boric acid induced Nrf2 nuclear translocation in wild-type mouse fibroblasts but not in Perk-null cells. Condition category: machinery_impairment nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: PERK was also needed for the measured movement of Nrf2 into the nucleus. organism: Mouse embryonic fibroblasts and human DU-145 cells tissue_or_cell_type: Cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4

evidence_span

{"source_cache": "artifacts/boron-research/36435196.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c", "start_char": 0, "end_char": 1651, "text_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c"}

experimental_model

Freshwater/seawater acclimation and Xenopus oocyte transporter expression

exposure

Freshwater versus seawater; boric-acid exposure during voltage clamp

limitations

Fish paralog is distinct from human SLC4A11. Borate uniport, boric-acid/OH cotransport and boric-acid/H exchange were not distinguished.

nutrient_topic

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

organism

Takifugu obscurus pufferfish; Xenopus expression host

plain_language

The fish kidney adjusts to the much greater boron exposure from seawater.

primary_references

[boron-p36435196] Seawater fish use an electrogenic boric acid transporter, Slc4a11A, for boric acid excretion by the kidney. (2023). https://pubmed.ncbi.nlm.nih.gov/36435196/ DOI: 10.1016/j.jbc.2022.102740

tissue_or_cell_type

Kidney tubular apical membrane and heterologous membrane

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 261–272

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Freshwater/seawater acclimation and Xenopus oocyte transporter expression · source_derived_draft · unverified_draft

### boron-pufferfish-renal-adaptation Seawater acclimation increased renal apical Slc4a11A expression and accompanied urine boric-acid concentrations of 19 mM versus 0.020 mM in freshwater fish. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The fish kidney adjusts to the much greater boron exposure from seawater. organism: Takifugu obscurus pufferfish; Xenopus expression host tissue_or_cell_type: Kidney tubular apical membrane and heterologous membrane experimental_model: Freshwater/seawater acclimation and Xenopus oocyte transporter expression limitations: Fish paralog is distinct from human SLC4A11. Borate uniport, boric-acid/OH cotransport and boric-acid/H exchange were not distinguished. exposure: Freshwater versus seawater; boric-acid exposure during voltage clamp evidence_span: {"source_cache": "artifacts/boron-research/36435196.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c", "start_char": 0, "end_char": 1651, "text_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c"} [boron-p36435196] Seawater fish use an electrogenic boric acid transporter, Slc4a11A, for boric acid excretion by the kidney. (2023). https://pubmed.ncbi.nlm.nih.gov/36435196/ DOI: 10.1016/j.jbc.2022.102740

evidence_span

{"source_cache": "artifacts/boron-research/36435196.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c", "start_char": 0, "end_char": 1651, "text_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c"}

experimental_model

Freshwater/seawater acclimation and Xenopus oocyte transporter expression

exposure

Freshwater versus seawater; boric-acid exposure during voltage clamp

limitations

Fish paralog is distinct from human SLC4A11. Borate uniport, boric-acid/OH cotransport and boric-acid/H exchange were not distinguished.

nutrient_topic

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

organism

Takifugu obscurus pufferfish; Xenopus expression host

plain_language

A fish version really did transport boric-acid equivalents in this experiment; that does not validate the disputed human assignment.

primary_references

[boron-p36435196] Seawater fish use an electrogenic boric acid transporter, Slc4a11A, for boric acid excretion by the kidney. (2023). https://pubmed.ncbi.nlm.nih.gov/36435196/ DOI: 10.1016/j.jbc.2022.102740

tissue_or_cell_type

Kidney tubular apical membrane and heterologous membrane

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 248–259

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Freshwater/seawater acclimation and Xenopus oocyte transporter expression · source_derived_draft · unverified_draft

### boron-pufferfish-transporter Pufferfish Slc4a11A expression increased boron accumulation, intracellular pH and outward currents during boric-acid exposure in oocytes, independently of extracellular sodium. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A fish version really did transport boric-acid equivalents in this experiment; that does not validate the disputed human assignment. organism: Takifugu obscurus pufferfish; Xenopus expression host tissue_or_cell_type: Kidney tubular apical membrane and heterologous membrane experimental_model: Freshwater/seawater acclimation and Xenopus oocyte transporter expression limitations: Fish paralog is distinct from human SLC4A11. Borate uniport, boric-acid/OH cotransport and boric-acid/H exchange were not distinguished. exposure: Freshwater versus seawater; boric-acid exposure during voltage clamp evidence_span: {"source_cache": "artifacts/boron-research/36435196.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c", "start_char": 0, "end_char": 1651, "text_sha256": "f33e845c95cab0ebe899c99562ebb23f43292cbab645601a5ab51a421fdc5f8c"} [boron-p36435196] Seawater fish use an electrogenic boric acid transporter, Slc4a11A, for boric acid excretion by the kidney. (2023). https://pubmed.ncbi.nlm.nih.gov/36435196/ DOI: 10.1016/j.jbc.2022.102740

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

The researchers tested the B2-depletion explanation and did not find support for it.

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 1158–1169

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-toxicity-not-b2-depletion The rat toxicity study found neither tissue-flavin changes nor overt riboflavin-deficiency signs supporting B2 depletion as the cause of boric-acid testicular toxicity. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The researchers tested the B2-depletion explanation and did not find support for it. 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/boron-research/42012780.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "673f9c1649ebaea729fb8331f6394dcad15d21b7bea8e6414542210b8e9fdd69", "start_char": 6857, "end_char": 8798, "text_sha256": "09a30283b0d51a099a2687875db729353a5f03f83f616c974d75a284679f1f8f"}

experimental_model

Negative-ion electrospray mass spectrometry

exposure

200 µM riboflavin and 400 µM boric acid in WAT solvent at pH 10.3

limitations

Nominal mass is consistent with, but does not uniquely establish, the proposed 1:1 structure. No site-resolving NMR or in-vivo binding measurement; signal intensity is not a bound fraction.

nutrient_topic

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

organism

Cell-free chemistry

plain_language

A laboratory signal suggests boron can attach to vitamin B2; this does not prove that usual boron intake depletes B2.

primary_references

[boron-p42012780] Identification of a Riboflavin-Boric Acid Complex by Electrospray Ionization Mass Spectrometry. (2026). https://pubmed.ncbi.nlm.nih.gov/42012780/ DOI: 10.1007/s12011-026-05110-9

tissue_or_cell_type

Purified riboflavin in alkaline solvent

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 183–194

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Negative-ion electrospray mass spectrometry · source_derived_draft · unverified_draft

### boron-riboflavin-adduct An additional m/z 401.3 ion was consistent with a 1:1 riboflavin–boric-acid complex in alkaline electrospray experiments; the ribityl binding site was not resolved. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A laboratory signal suggests boron can attach to vitamin B2; this does not prove that usual boron intake depletes B2. organism: Cell-free chemistry tissue_or_cell_type: Purified riboflavin in alkaline solvent experimental_model: Negative-ion electrospray mass spectrometry limitations: Nominal mass is consistent with, but does not uniquely establish, the proposed 1:1 structure. No site-resolving NMR or in-vivo binding measurement; signal intensity is not a bound fraction. exposure: 200 µM riboflavin and 400 µM boric acid in WAT solvent at pH 10.3 evidence_span: {"source_cache": "artifacts/boron-research/42012780.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "673f9c1649ebaea729fb8331f6394dcad15d21b7bea8e6414542210b8e9fdd69", "start_char": 6857, "end_char": 8798, "text_sha256": "09a30283b0d51a099a2687875db729353a5f03f83f616c974d75a284679f1f8f"} [boron-p42012780] Identification of a Riboflavin-Boric Acid Complex by Electrospray Ionization Mass Spectrometry. (2026). https://pubmed.ncbi.nlm.nih.gov/42012780/ DOI: 10.1007/s12011-026-05110-9