Seitz H K, Czygan P, Waldherr R, Veith S, Raedsch R, Kässmodel H, Kommerell B
Gastroenterology. 1984 May;86(5 Pt 1):886-91.
The incidence, distribution, size, and histopathology of grossly visible intestinal tumors induced by the parenteral administration of 1,2-dimethylhydrazine dihydrochloride were examined in 32 paired rats fed a nutritionally adequate liquid diet containing 36% of total calories either as ethanol or isocaloric carbohydrates. The liquid diets were begun 4 wk before the first of four weekly injections of 1,2-dimethylhydrazine dihydrochloride. At the time of the subcutaneous application of the procarcinogen, liquid diets were omitted for 3 wk, and were replaced by a standard laboratory diet. This feeding schedule was repeated four times, and after 32 wk the animals were killed. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs. 6, p less than 0.02). However, alcohol had no effect on tumor size or histopathology. Chronic ethanol ingestion did not exhibit any cocarcinogenic effect in tissues other than the rectum. A 47% increase in the activity of mucosal alcohol dehydrogenase in the distal colorectum was found between chronically ethanol-fed rats and pair-fed controls (0.241 +/- 0.019 vs. 0.164 +/- 0.020 mumol X mg protein-1 X h-1, p less than 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Fecal bile acids, however, do not play a role as promoters of rectal cancer under the present experimental conditions. The data give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.
在32对大鼠中，研究了经肠胃外给予二盐酸1,2 - 二甲基肼诱导的肉眼可见肠道肿瘤的发生率、分布、大小及组织病理学。这些大鼠喂食营养充足的液体饮食，其中36%的总热量由乙醇或等热量碳水化合物提供。液体饮食在首次每周注射四次二盐酸1,2 - 二甲基肼前4周开始。在皮下应用前致癌物时，液体饮食停用3周，改为标准实验室饮食。这种喂食方案重复四次，32周后处死动物。长期摄入乙醇显著增加了直肠肿瘤的总数（17个对6个，p小于0.02）。然而，乙醇对肿瘤大小或组织病理学没有影响。长期摄入乙醇在直肠以外的组织中未表现出任何促癌作用。长期喂食乙醇的大鼠与配对喂食的对照组相比，远端结肠直肠黏膜乙醇脱氢酶活性增加了47%（分别为0.241±0.019对0.164±0.020 μmol·mg蛋白⁻¹·h⁻¹，p小于0.01）。这可能部分解释了乙醇在该组织中的促癌作用。然而，在本实验条件下，粪便胆汁酸并非直肠癌的促癌因素。这些数据为酒精性直肠癌症发病率增加的流行病学发现提供了实验支持。
