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. 2003 Nov;111(14):1699–1703. doi: 10.1289/ehp.6229

Oxidative stress-related mechanisms are associated with xenobiotics exerting excess toxicity to Fanconi anemia cells.

Giovanni Pagano 1, Paola Manini 1, Debasis Bagchi 1
PMCID: PMC1241709  PMID: 14594617

Abstract

An extensive body of evidence has demonstrated the sensitivity of Fanconi anemia (FA) cells to redox-active xenobiotics, such as mitomycin C, diepoxybutane, cisplatin, and 8-methoxypsoralen plus ultraviolet irradiation, with toxicity mechanisms that are consistent with a deficiency of FA cells in coping with oxidative stress. A recent study has reported on excess sensitivity of FA complementation A group cells to chromium VI [Cr(VI)] toxicity, by postulating that a deficiency in Cr-DNA cross-link removal by FA cells and formation of Cr(VI)-associated cross-links may be the mechanism of Cr(VI)-induced cytotoxicity. However, the report failed to demonstrate any enhanced Cr uptake or, especially, any increase in Cr-DNA adducts. Thus, well-established findings on Cr(VI)-induced oxidative stress may explain excess sensitivity of FA cells to Cr(VI) in terms of its inability to cope with the Cr(VI)-induced prooxidant state.

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Selected References

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