Selenium suppresses the metabolism of benzo[a]pyrene by rat-liver extracts, and exerts a dual effect on its mutagenicity.
Liver homogenates from rats injected with 3-methylcholanthrene were employed for metabolism of benzo[a]pyrene (BP) and in assays of aryl hydrocarbon hydroxylase (AHH) activity in vitro. Sodium selenite inhibited AHH activity to a maximum of approximately 70%. It suppressed the overall metabolism of benzo[a]pyrene; a distinct reduction in the products was evident on h.p.l.c. analysis. Sodium thiosulphate also inhibited AHH activity by approximately 47%. Inclusion of S2O3(2-) and SeO3(2-), in combination, led to a cumulative inhibition of 87%. The mutagenicity of BP in the Salmonella auxotroph reversion system (Ames test) was enhanced by SeO3(2-) at concentrations below 0.2 mM. Above this level a significant antimutagenic effect was observed.
D000818:Animals; D001564:Benzo(a)pyrene / Q000378:metabolism* / Q000494:pharmacology; D001579:Benzopyrene Hydroxylase / Q000037:antagonists & inhibitors; D006900:Hydroxylation; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009153:Mutagens; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000494:pharmacology*
D009153:Mutagens; D001564:Benzo(a)pyrene; D001579:Benzopyrene Hydroxylase; D012643:Selenium