Chromate / chromium(VI) oxyanion

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}

experimental_model

Ascorbate restoration and ATM perturbation in human lung-cell cultures

exposure

Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing

limitations

Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.

nutrient_topic

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

organism

Human H460 cells and normal lung fibroblasts

plain_language

This downstream damage-response protein changed in the low-ascorbate culture condition.

primary_references

[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

tissue_or_cell_type

DNA-damage signaling

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1134–1145

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

### chromium-chromate-chk2 Chromate exposure induced CHK2 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}

experimental_model

Ascorbate restoration and ATM perturbation in human lung-cell cultures

exposure

Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing

limitations

Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.

nutrient_topic

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

organism

Human H460 cells and normal lung fibroblasts

plain_language

This downstream damage-response protein changed in the low-ascorbate culture condition.

primary_references

[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

tissue_or_cell_type

DNA-damage signaling

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1147–1158

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

### chromium-chromate-kap1 Chromate exposure induced KAP1 phosphorylation as part of the ATM response in standard ascorbate-poor human cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream damage-response protein changed in the low-ascorbate culture condition. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

evidence_span

{"source_cache": "artifacts/chromium-research/17263387.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35", "start_char": 0, "end_char": 1638, "text_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35"}

experimental_model

X-ray absorption and EPR before and after cell fractionation

exposure

Cr(VI)-treated cells; comparisons with model Cr(III) complexes

limitations

The artifact evidence concerns chromium(VI)-exposed cells and the tested isolation procedures. It does not negate the activity measured when an isolated peptide preparation is added to an enzyme assay.

nutrient_topic

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

organism

Human A549/HepG2, hamster V79 and mouse C2C12 cells

plain_language

Some apparent chromodulin-like material formed during sample preparation, raising doubts about its identity as a pre-existing cellular signal.

primary_references

[chromium-p17263387] X-ray absorption and EPR spectroscopic studies of the biotransformations of chromium(VI) in mammalian cells. Is chromodulin an artifact of isolation methods? (2007). https://pubmed.ncbi.nlm.nih.gov/17263387/ DOI: 10.1021/ja063792r

tissue_or_cell_type

Intact and lysed cell preparations

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 237–248

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray absorption and EPR before and after cell fractionation · source_derived_draft · unverified_draft

### chromium-chromodulin-isolation-artifact Most Cr(III) formed in Cr(VI)-treated cells was associated with high-molecular-mass ligands; cell lysis redistributed chromium into a low-molecular-weight fraction spectroscopically similar to reported chromodulin. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some apparent chromodulin-like material formed during sample preparation, raising doubts about its identity as a pre-existing cellular signal. organism: Human A549/HepG2, hamster V79 and mouse C2C12 cells tissue_or_cell_type: Intact and lysed cell preparations experimental_model: X-ray absorption and EPR before and after cell fractionation limitations: The artifact evidence concerns chromium(VI)-exposed cells and the tested isolation procedures. It does not negate the activity measured when an isolated peptide preparation is added to an enzyme assay. exposure: Cr(VI)-treated cells; comparisons with model Cr(III) complexes evidence_span: {"source_cache": "artifacts/chromium-research/17263387.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35", "start_char": 0, "end_char": 1638, "text_sha256": "912905b2fefe0745017faae62124fe077d3944cde635ae1012ff76fc33094b35"} [chromium-p17263387] X-ray absorption and EPR spectroscopic studies of the biotransformations of chromium(VI) in mammalian cells. Is chromodulin an artifact of isolation methods? (2007). https://pubmed.ncbi.nlm.nih.gov/17263387/ DOI: 10.1021/ja063792r

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"}

experimental_model

Ascorbate restoration and ATM perturbation in human lung-cell cultures

exposure

Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing

limitations

Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium.

nutrient_topic

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

organism

Human H460 cells and normal lung fibroblasts

plain_language

Vitamin C availability changed which damage-response pathway the toxic exposure activated.

primary_references

[chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

tissue_or_cell_type

DNA-damage signaling

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1121–1132

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ascorbate restoration and ATM perturbation in human lung-cell cultures · source_derived_draft · unverified_draft

### chromium-ascorbate-atm-context Ascorbate restoration prevented Cr(VI)-induced ATM activation observed in standard ascorbate-poor human lung-cell cultures. Condition category: nutrient_deficiency nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C availability changed which damage-response pathway the toxic exposure activated. organism: Human H460 cells and normal lung fibroblasts tissue_or_cell_type: DNA-damage signaling experimental_model: Ascorbate restoration and ATM perturbation in human lung-cell cultures limitations: Cr(VI) toxicology, not an experiment with dietary Cr(III). Loss of ATM activation does not mean loss of all genotoxicity or that vitamin C universally detoxifies chromium. exposure: Chromate exposure in standard ascorbate-poor versus ascorbate-restored cells; ATM inhibition/silencing evidence_span: {"source_cache": "artifacts/chromium-research/25977998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3", "start_char": 0, "end_char": 2163, "text_sha256": "26c325e343b04aa77acf3164d848e8127c2d6a329ff0d9968426a12bde81d0b3"} [chromium-p25977998] Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics. (2016). https://pubmed.ncbi.nlm.nih.gov/25977998/ DOI: 10.1289/ehp.1409434

evidence_span

{"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"}

experimental_model

Cell-free chromate reduction followed by plasmid replication in human fibroblasts

exposure

2 versus 5 mM glutathione with Cr(VI)

limitations

Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations.

nutrient_topic

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

organism

Chemical system with human fibroblast mutagenicity readout

plain_language

The authors detected and assigned a glutathione-linked DNA lesion; the preparation and analytical assignment matter.

primary_references

[chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g

tissue_or_cell_type

DNA reaction mixture and reporter plasmid

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1173–1184

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free chromate reduction followed by plasmid replication in human fibroblasts · source_derived_draft · unverified_draft

### chromium-gsh-chromate-adducts The study attributed about 5% of total chromium-DNA adducts to GSH-Cr-DNA crosslinks at 2 mM glutathione, with four- to fivefold higher crosslinking at 5 mM. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The authors detected and assigned a glutathione-linked DNA lesion; the preparation and analytical assignment matter. organism: Chemical system with human fibroblast mutagenicity readout tissue_or_cell_type: DNA reaction mixture and reporter plasmid experimental_model: Cell-free chromate reduction followed by plasmid replication in human fibroblasts limitations: Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations. exposure: 2 versus 5 mM glutathione with Cr(VI) evidence_span: {"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"} [chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g

evidence_span

{"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"}

experimental_model

Cell-free chromate reduction followed by plasmid replication in human fibroblasts

exposure

2 versus 5 mM glutathione with Cr(VI)

limitations

Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations.

nutrient_topic

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

organism

Chemical system with human fibroblast mutagenicity readout

plain_language

More glutathione did not simply mean less damage in this chemical system.

primary_references

[chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g

tissue_or_cell_type

DNA reaction mixture and reporter plasmid

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 1160–1171

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free chromate reduction followed by plasmid replication in human fibroblasts · source_derived_draft · unverified_draft

### chromium-gsh-chromate-mutagenesis Chromate reduction with 2 mM glutathione produced weak plasmid mutagenicity; 5 mM glutathione produced about four times the mutation yield per DNA adduct. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glutathione did not simply mean less damage in this chemical system. organism: Chemical system with human fibroblast mutagenicity readout tissue_or_cell_type: DNA reaction mixture and reporter plasmid experimental_model: Cell-free chromate reduction followed by plasmid replication in human fibroblasts limitations: Toxicology assay, not oral chromium exposure. Proposed crosslink identities depend on preparation and analytical methods; later work questions some pre-reacted ternary-adduct preparations. exposure: 2 versus 5 mM glutathione with Cr(VI) evidence_span: {"source_cache": "artifacts/chromium-research/18808157.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb", "start_char": 0, "end_char": 1724, "text_sha256": "ed2c80b5da41d110da38bc0ed29d900d1d33f4180b64e13cb9b24ae7da5e1cdb"} [chromium-p18808157] Reduction with glutathione is a weakly mutagenic pathway in chromium(VI) metabolism. (2008). https://pubmed.ncbi.nlm.nih.gov/18808157/ DOI: 10.1021/tx800265g