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Ataxia telangeictasia

DNA Repair (Amst). 2004 Oct 5;3(10):1263-72.  Related Articles, Links  

Iron chelators increase the resistance of Ataxia telangeictasia cells to
oxidative stress.

Shackelford RE, Manuszak RP, Johnson CD, Hellrung DJ, Link CJ, Wang S.

Iowa Cancer Research Foundation, 11043 Aurora Avenue, Urbandale, IA 50322, USA.

Ataxia telangeictasia (A-T) is an autosomal recessive disorder characterized by
immune dysfunction, genomic instability, chronic oxidative damage, and
increased cancer incidence. Previously, desferal was found to increase the
resistance of A-T, but not normal cells to exogenous oxidative stress in the
colony forming-efficiency assay, suggesting that iron metabolism is
dysregulated in A-T. Since desferal both chelates iron and modulates gene
expression, we tested the effects of apoferritin and the iron chelating
flavonoid quercetin on A-T cell colony-forming ability. We demonstrate that
apoferritin and quercetin increase the ability of A-T cells to form colonies.
We also show that labile iron levels are significantly elevated in
Atm-deficient mouse sera compared to syngeniec wild type mice. Our findings
support a role for labile iron acting as a Fenton catalyst in A-T, contributing
to the chronic oxidative stress seen in this disease. Our findings further
suggest that iron chelators might promote the survival of A-T cells and hence,
individuals with A-T.

PMID: 15336622 [PubMed - in process]

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