Role of glutathione in liver-mediated mutagenicity of acrylonitrile.
The mutagenic activity of acrylonitrile (ACN) towards the Salmonella typhimurium strain TA1530 was evaluated after a short preincubation time in liquid medium in the presence of microsomes, cytosolic fractions and post-mitochondrial fractions of liver from untreated and phenobarbitone (PB)-pretreated rats and mice. The effect of the presence of glutathione (GSH) was also examined. GSH enhanced the microsomal-mediated mutagenicity of ACN; that effect was abolished in the presence of CO. The effect of GSH was usually greater after pretreatment by phenobarbitone. Other sulfhydryl compounds induce a weaker mutagenic activity than GSH. These observations support the hypothesis of a mediated formation of a mutagen involving GSH, but the adduct between ACN an GSH was not mutagenic.
D000181:Acrylonitrile / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D001711:Biotransformation; D002248:Carbon Monoxide / Q000494:pharmacology; D005978:Glutathione / Q000502:physiology*; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D009152:Mutagenicity Tests; D009153:Mutagens; D009570:Nitriles / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D012486:Salmonella typhimurium / Q000235:genetics
D009153:Mutagens; D009570:Nitriles; D002248:Carbon Monoxide; D005978:Glutathione; D000181:Acrylonitrile