Consequences of acrylonitrile metabolism in rat hepatocytes: effects on lipid peroxidation and viability of the cells.
Acrylonitrile caused thiobarbituric acid-positive reactants time- and concentration-dependently in isolated hepatocytes. This effect was markedly enhanced by gassing of the medium with 95% oxygen-5% CO2 gas mixture. Glycidonitrile, an acrylonitrile metabolite, proved more potent in this respect than the parent acrylonitrile or its end metabolite, cyanide anion. The latter decreased greatly the viability of isolated liver cells but caused thiobarbituric acid-positive reactants only in the presence of diethylmaleate. Acrylonitrile caused also a decrease in the concentration of nonprotein sulfhydryl groups but the oxidation of glutathione (GSH) to GSSG (oxidized glutathione) was not the major mechanism. This might indicate the consumption of GSH in the glutathione S-transferase catalyzed reactions. In contrast to cyanide anion-induced effects acrylonitrile did not affect markedly the viability of hepatocytes.
D000181:Acrylonitrile / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009570:Nitriles / Q000633:toxicity*; D010100:Oxygen / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011190:Potassium Cyanide / Q000494:pharmacology; D051381:Rats; D013438:Sulfhydryl Compounds / Q000378:metabolism
D008054:Lipid Peroxides; D009570:Nitriles; D013438:Sulfhydryl Compounds; D002245:Carbon Dioxide; C011700:carbogen; D005982:Glutathione Transferase; D005978:Glutathione; D000181:Acrylonitrile; D011190:Potassium Cyanide; D010100:Oxygen