Studies on dioxin (TCDD) carcinogenicity in humans have yielded conflicting results. One possible explanation of these mixed findings rests on the role of susceptibility factors. We are currently addressing this hypothesis in a case-control study in the Seveso population. In a pilot investigation, a set of susceptibility markers have been measured in 20 healthy volunteers. Ethoxyresorufin-O-Deethylase (EROD) activity was significantly greater in subjects with mutant CYP1a1 genotypes than in homozygous wild type subjects. No difference in mRNA expression was noted. Meat consumption possibly influences this result. Suggestions of an interaction between "mutation" and "TCDD induction" were obtained. © 1993.
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