Lipid peroxidation and ethanol-related tumor promotion in Fischer-344 rats treated with tobacco-specific nitrosamines.

摘要: Male Fischer-344 rats were treated, by gavage, with a total dose of 40 mmol/kg N′ nitrosonomicotine (NNN) or 20 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), three times week for 4 weeks. One afterwards the fed an isocaloric liquid diet containing 7% (v/v) ethanol and continued on this until killed. Cumulative ethane exhaled rat 180 mm was measured at 54 weeks start study found to increase significantly ( P < 0.001) either NNN NNK treatment but more so when followed consumption. Other indices lipid peroxidation, cholesterol phospholipids in extracts from liver, esophagus lungs 55 Ethanol consumption increased amount per g tissue naive NNN- NNK-treated rats. All peroxidative measured, i.e. malondialdehyde (MDA), diene- triene-conjugates fluorescence, main metabolic Site, whether they treated remained untreated. Overall, peroxidation also showed other tissues, results differed different indices. The differences may be due peroxidalion products their rates production degradation conversion products. However, largest increases seen Incidence tumors tissues assessed about two-fold esophagus, oral cavity, liver induced NNK. caused mean frequency size induced. suggest that ethanol-relaxed promotion NNK-induced result target tissue.