12个月前对大鼠进行致癌预处理可抑制乙醇诱导的乙烷呼出。
Inhibition of ethanol induced ethane exhalation by carcinogenic pretreatment of rats 12 months earlier.
作者信息
Szebeni J, Eskelson C D, Mufti S I, Watson R R, Sipes I G
出版信息
Life Sci. 1986 Dec 29;39(26):2587-91. doi: 10.1016/0024-3205(86)90113-x.
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.
用呼出乙烷作为衡量大鼠体内脂质过氧化的指标，这些大鼠先用肝癌致癌物二乙基亚硝胺处理，随后用2-乙酰氨基芴（AAF）和四氯化碳处理，随后喂食含7%乙醇的流质饮食12个月。其他组包括用甲基苄基亚硝胺（MBN，一种食管致癌物）处理的动物，或经非致癌物预处理且有或没有喂食7%乙醇的动物。无论是否用MBN预处理，摄入乙醇的大鼠体内乙烷生成量都会增加。与之形成鲜明对比的是，接受肝癌致癌方案处理的大鼠中不存在乙醇诱导的乙烷生成增加现象。我们的结果强化了最近的观察结果，即肿瘤细胞对脂质过氧化的敏感性降低。此外，它们证实了存在争议的概念，即乙醇摄入后脂质过氧化会增加。
Zotero 插件