Abstract
Sodium selenite induces substantial DNA damage in human fibroblasts. This damage appears to consist of true DNA breaks rather than alkali-labile sites and to not arise via free oxygen radical production. Cloning efficiency and DNA strand breakage show dramatically enhanced sensitivity to selenite if the treatments are carried out in the presence of reduced glutathione or, to a lesser degree, serum, supporting the notion that a glutathione-selenite conjugant is required for activation to a genotoxic form. In addition, the notion that selenium anticarcinogenicity involves enhancement of cellular DNA repair, has been examined. No evidence for enhancement (or inhibition) of repair of methyl methanesulfonate (MMS)-, UV- or bleomycin-induced DNA damage was observed in human fibroblasts treated with selenite.
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