Cyclic ADP-ribose

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

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

cross_nutrient

true

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"}

experimental_model

Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay

exposure

CD38 cDNA transfection; NAD+ extracellular substrate

limitations

This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human protein; African green monkey cells; sea urchin microsomes

plain_language

A CD38-generated messenger mobilized calcium in an egg-microsome bioassay.

primary_references

[b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d

tissue_or_cell_type

COS1 kidney-cell culture; sea-urchin egg microsomes

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 607–619

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay · source_derived_draft · unverified_draft

### b3-cons-cadpr-store-calcium Extracellular cyclic ADP-ribose generated by human CD38-expressing COS1 cells was detected by calcium release from sea-urchin egg microsomes. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A CD38-generated messenger mobilized calcium in an egg-microsome bioassay. organism: Human protein; African green monkey cells; sea urchin microsomes tissue_or_cell_type: COS1 kidney-cell culture; sea-urchin egg microsomes experimental_model: Human CD38 expression in monkey COS1 cells with sea-urchin microsome bioassay limitations: This mixed-species bioassay does not demonstrate intracellular trafficking of extracellular cADPR or calcium regulation after oral niacin. exposure: CD38 cDNA transfection; NAD+ extracellular substrate cross_nutrient: true evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381993.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 540, "file_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5", "text_sha256": "e8ba405a5300f922bcf34c358d95735b86637331f4cf15a009ac5bf8df93f1e5"} [b3-cons-cd381993] Human lymphocyte antigen CD38 catalyzes the production of cyclic ADP-ribose. (1993). https://pubmed.ncbi.nlm.nih.gov/8253202/ DOI: 10.1016/0014-5793(93)80735-d

cross_nutrient

false

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"}

experimental_model

Biochemical characterization of human CD38

exposure

Cyclic ADP-ribose substrate

limitations

Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human

plain_language

CD38 also breaks down cyclic ADP-ribose.

primary_references

[b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383

tissue_or_cell_type

Cell-free enzyme preparation

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 593–605

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical characterization of human CD38 · source_derived_draft · unverified_draft

### b3-cons-cd38-cadpr-hydrolysis Human CD38 also hydrolyzes cyclic ADP-ribose to ADP-ribose. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: CD38 also breaks down cyclic ADP-ribose. organism: Human tissue_or_cell_type: Cell-free enzyme preparation experimental_model: Biochemical characterization of human CD38 limitations: Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes. exposure: Cyclic ADP-ribose substrate cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"} [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383

cross_nutrient

false

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"}

experimental_model

Biochemical characterization of human CD38

exposure

NAD+ as substrate

limitations

Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human

plain_language

Some CD38 cleavage produces the cyclic calcium messenger.

primary_references

[b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383

tissue_or_cell_type

Cell-free enzyme preparation

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 579–591

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical characterization of human CD38 · source_derived_draft · unverified_draft

### b3-cons-cd38-cyclization Human CD38 produces cyclic ADP-ribose as a low-efficiency branch of NAD+ cleavage. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some CD38 cleavage produces the cyclic calcium messenger. organism: Human tissue_or_cell_type: Cell-free enzyme preparation experimental_model: Biochemical characterization of human CD38 limitations: Primary human enzyme study; source abstract used. Product proportions are assay-specific and do not establish tissue flux or supplementation outcomes. exposure: NAD+ as substrate cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/cd381998.abstract.txt", "locator": "Indexed abstract", "start_char": 0, "end_char": 1755, "file_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad", "text_sha256": "39f90bb382ddfee34e808fc93c5a1afafc1d9638a9dc73f2770e815827b4f2ad"} [b3-cons-cd381998] Human CD38 is an authentic NAD(P)+ glycohydrolase. (1998). https://pubmed.ncbi.nlm.nih.gov/9494110/ DOI: 10.1042/bj3301383

cross_nutrient

false

evidence_span

{"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"}

experimental_model

Purified human SARM1 TIR domain; HPLC and LC-MS/MS

exposure

NAD+ incubation

limitations

Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. Drosophila product ratios differed and are not generalized to humans.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Human

plain_language

The human SARM1 reaction also makes some cyclic ADP-ribose.

primary_references

[b3-cons-sarm2017] The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration. (2017). https://pubmed.ncbi.nlm.nih.gov/28334607/ DOI: 10.1016/j.neuron.2017.02.022

tissue_or_cell_type

Cell-free preparation

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 691–703

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human SARM1 TIR domain; HPLC and LC-MS/MS · source_derived_draft · unverified_draft

### b3-cons-sarm-cadpr Human SARM1 TIR-domain NAD+ cleavage also generated cyclic ADP-ribose as a minor product. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human SARM1 reaction also makes some cyclic ADP-ribose. organism: Human tissue_or_cell_type: Cell-free preparation experimental_model: Purified human SARM1 TIR domain; HPLC and LC-MS/MS limitations: Purified engineered TIR fragment rather than basal activity of intact full-length SARM1; no dietary dose inference. Drosophila product ratios differed and are not generalized to humans. exposure: NAD+ incubation cross_nutrient: false evidence_span: {"source_cache": "artifacts/niacin-consumption-sources/sarm2017.txt", "locator": "Full text, normalized paragraph 24", "start_char": 15550, "end_char": 16946, "file_sha256": "fc30de231911f5c30425173d684495e62c725ba27c78d44592e6bc68433ef545", "text_sha256": "9a9b91a772186c34d8b6305a04bbcf6d3acc40b0448e6f478811527c5174981e"} [b3-cons-sarm2017] The SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD+ Cleavage Activity that Promotes Pathological Axonal Degeneration. (2017). https://pubmed.ncbi.nlm.nih.gov/28334607/ DOI: 10.1016/j.neuron.2017.02.022

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

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/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