Weidema W F, Deschner E E, Cohen B I, DeCosse J J
J Natl Cancer Inst. 1985 Mar;74(3):665-70.
The acute effects of cholic acid ingestion on methylazoxymethanol acetate [(MAM) CAS: 592-62-1]-treated conventional and germfree rats were investigated. Male SD rats were divided into 4 treatment groups. The first group received control chow; the second group, control chow plus 0.5% cholic acid; the third group, control chow plus MAM; and the fourth group, control chow plus 0.5% cholic acid plus MAM. Fecal bile acids, cholesterol, cholesteral degradation products, and neutral sterols, as well as labeling indices and numbers of epithelial cells per crypt column, were measured after 6 weeks of treatment. The administration of MAM to germfree groups diminished both fecal bulk and the amount of fecal water. MAM did not affect the fecal bile acid composition. Analysis of the fecal bile acids in conventional rats fed cholic acid demonstrated that half of the bile acids were in a form of deoxycholic acid. In the germfree groups fed cholic acid, 90% of the bile acids appeared unaltered in the feces. Neither in the germfree nor in the conventional groups was an effect seen of MAM on the output of fecal neutral sterols. The addition of cholic acid to the food decreased the output of neutral sterols both in the conventional (P less than .001) and in the germfree (P less than .02) animals. The germfree animals showed a reduced amount of neutral steroid excretion (P less than .01) when compared to the findings for the conventional groups. MAM had no influence on the fecal cholesterol or coprostanol output. The consumption of 0.5% cholic acid decreased the total output of cholesterol (P less than .05). The excretion of coprostanol was significantly diminished in the conventional rats fed cholic acid (P less than .001). No difference in labeling indices was observed between conventional and germfree rats, whether treated with cholic acid, MAM, or cholic acid plus MAM. However, all germfree groups showed less epithelial cells per crypt column (P less than .001) than did conventional animals.
研究了胆酸摄入对经乙酸甲基偶氮甲醇[(MAM)，CAS: 592-62-1]处理的普通大鼠和无菌大鼠的急性影响。雄性SD大鼠分为4个处理组。第一组给予对照饲料；第二组，对照饲料加0.5%胆酸；第三组，对照饲料加MAM；第四组，对照饲料加0.5%胆酸加MAM。治疗6周后，测量粪便胆汁酸、胆固醇、胆固醇降解产物和中性固醇，以及隐窝柱的标记指数和上皮细胞数量。给无菌组大鼠施用MAM可减少粪便体积和粪便水量。MAM不影响粪便胆汁酸组成。对喂食胆酸的普通大鼠粪便胆汁酸的分析表明，一半的胆汁酸以脱氧胆酸的形式存在。在喂食胆酸的无菌组中，90%的胆汁酸在粪便中未发生改变。无论是无菌组还是普通组，均未观察到MAM对粪便中性固醇排出量的影响。在食物中添加胆酸可降低普通动物（P<0.001）和无菌动物（P<0.02）的中性固醇排出量。与普通组的结果相比，无菌动物的中性类固醇排泄量减少（P<0.01）。MAM对粪便胆固醇或粪甾烷醇排出量没有影响。摄入0.5%胆酸可降低胆固醇的总排出量（P<0.05）。喂食胆酸的普通大鼠中粪甾烷醇的排泄量显著减少（P<0.001）。无论用胆酸、MAM或胆酸加MAM处理，普通大鼠和无菌大鼠之间的标记指数均未观察到差异。然而，所有无菌组的每个隐窝柱上皮细胞数量均比普通动物少（P<0.001）。
