ArticleEnvironmental health perspectives2003
Oxidative stress-related mechanisms are associated with xenobiotics exerting excess toxicity to Fanconi anemia cells.
Article in Environmental health perspectives, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Circadian rhythm and aryl hydrocarbon receptor crosstalk in bone marrow adipose tissue and implications in leukemia.Scientific reports · 2025Article
- Reduction of TRPC1/TRPC3 mediated CaCellular signalling · 2023Article
- Toxicological effects of major environmental pollutants: an overview.Environmental monitoring and assessment · 2013Review
- Formation of cyclophosphamide specific DNA adducts in hematological diseases.Pediatric blood & cancer · 2012Article
- Amifostine protection against mitomycin-induced chromosomal breakage in fanconi anaemia lymphocytes.Molecules (Basel, Switzerland) · 2008Article
- Diepoxybutane activates the mitochondrial apoptotic pathway and mediates apoptosis in human lymphoblasts through oxidative stress.Toxicology in vitro : an international journal published in association with BIBRA · 2007Article
- Protein oxidation implicated as the primary determinant of bacterial radioresistance.PLoS biology · 2007Article
- A never-ending story: the steadily growing family of the FA and FA-like genes.Genetics and molecular biologyArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
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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