Seitz H K, Czygan P, Simanowski U, Waldherr R, Veith S, Raedsch R, Kommerell B
Alcohol Alcohol. 1985;20(4):427-33.
The effect of chronic ethanol administration on 1, 2-dimethylhydrazine-induced rectal carcinogenesis was investigated in 32 paired male Sprague-Dawley rats fed a nutritionally-adequate liquid diet containing 36% of the total calories as either ethanol or isocaloric carbohydrates. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs 6; P less than 0.02), whereas no cocarcinogenic effect of ethanol was observed in other parts of the intestine. Alcohol did not influence tumor size or histopathology. A 47% increase in the activity of mucosal alcohol dehydrogenase in the distal colorectal region was found between chronically-ethanol-fed rats and pair-fed controls (0.241 +/- 0.019 vs 0.164 +/- 0.020 mumol/mg of protein/hr; P less than 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Faecal bile acids, however, do not play a role as promotors of rectal carcinogenesis under the present experimental conditions. The results give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.
在32对雄性斯普拉格-道利大鼠中研究了长期给予乙醇对1,2-二甲基肼诱导的直肠癌发生的影响，这些大鼠喂食营养充足的液体饮食，其中36%的总热量来自乙醇或等热量的碳水化合物。长期摄入乙醇显著增加了直肠肿瘤的总数（17个对6个；P<0.02），而在肠道的其他部位未观察到乙醇的促癌作用。乙醇不影响肿瘤大小或组织病理学。长期喂食乙醇的大鼠与配对喂食的对照组相比，远端结肠直肠区域黏膜乙醇脱氢酶的活性增加了47%（分别为0.241±0.019对0.164±0.020μmol/mg蛋白质/小时；P<0.01）。这可能部分解释了乙醇在该组织中的促癌作用。然而，在目前的实验条件下，粪便胆汁酸并不作为直肠癌发生的促进剂起作用。这些结果为酒精性患者直肠癌发病率增加的流行病学发现提供了实验支持。
