Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics | Zendy

Michał W. Łuczak | Zendy; Samantha E. Green | Zendy; Anatoly Zhitkovich | Zendy

Open Access

Different ATM Signaling in Response to Chromium(VI) Metabolism via Ascorbate and Nonascorbate Reduction: Implications for in Vitro Models and Toxicogenomics

Author(s) -

Michał W. Łuczak,

Samantha E. Green,

Anatoly Zhitkovich

Publication year - 2015

Publication title -

environmental health perspectives

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.257

H-Index - 282

eISSN - 1552-9924

pISSN - 0091-6765

DOI - 10.1289/ehp.1409434

Subject(s) - hexavalent chromium , dna damage , microbiology and biotechnology , oxidative stress , glutathione , biology , clonogenic assay , chemistry , apoptosis , biochemistry , dna , enzyme , chromium , organic chemistry

Carcinogenic hexavalent chromium [Cr(VI)] requires cellular reduction to generate DNA damage. Metabolism of Cr(VI) by its principal reducer ascorbate (Asc) lacks a Cr(V) intermediate, which is abundant in reactions with a minor reducing agent, glutathione. Cultured cells are widely used in mechanistic studies of Cr(VI) toxicity; however, they typically contain < 1% of normal Asc levels. Asc deficiency is also expected to diminish protection against reactive oxygen species.

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