Inhibition of ethanol induced ethane exhalation by carcinogenic pretreatment of rats 12 months earlier.
The exhalation of ethane was used as a measure of in vivo lipid peroxidation in rats treated with the hepatocarcinogen diethylnitrosamine followed by 2-acetylaminofluorene (AAF), and carbon tetrachloride, and subsequently fed a liquid diet containing 7% ethanol for 12 months. The other groups consisted of animals treated with methylbenzylnitrosamine (MBN), an esophageal carcinogen, or non-carcinogen pretreated animals with or without 7% ethanol feeding. Ethane production was increased in rats consuming ethanol irrespective of their pretreatment with MBN. In sharp contrast, the ethanol-induced increase of ethane production was absent in rats given the hepatocarcinogenic regime. Our results strengthen recent observations indicating decreased susceptibility of tumor cells to lipid peroxidation. In addition, they confirm the debated concept that there is increased lipid peroxidation following ethanol consumption.
D015073:2-Acetylaminofluorene / Q000494:pharmacology; D000818:Animals; D001944:Breath Tests; D002251:Carbon Tetrachloride / Q000494:pharmacology; D002273:Carcinogens / Q000494:pharmacology*; D004052:Diethylnitrosamine / Q000494:pharmacology; D004347:Drug Interactions; D004980:Ethane / Q000378:metabolism*; D000431:Ethanol / Q000494:pharmacology*; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D002273:Carcinogens; D008054:Lipid Peroxides; D004052:Diethylnitrosamine; D000431:Ethanol; D015073:2-Acetylaminofluorene; D002251:Carbon Tetrachloride; D004980:Ethane