Abstract
Acrolein, a short-chain aldehyde encountered as a component of tobacco smoke and as a ubiquitous environmental contaminant, was tested for its toxic and mutagenic effects toward human fibroblast cells. We found that human cells characterized by a deficiency in DNA repair (cells from xeroderma pigmentosum (XP) patients) were much more sensitive ( D 37 ≌ 0.25 μM ) to the cytotoxic effects of acrolein than were cells from normal individuals ( D 37 ≌ 0.8 μM ). Acrolein was also strongly mutagenic to the XP cells (a dose response was observed between 0.2 and 0.8 μM acrolein); however acrolein did not induce an increase in the mutant frequency of normal fibroblasts. Possible reasons for this apparent lack of mutagenicity in normal human cells are discussed.
Published Version
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