Rao A V, Janezic S A, Friday D, Kendall C W
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Ontario, Canada.
Cancer Lett. 1992 Apr 30;63(3):249-57. doi: 10.1016/0304-3835(92)90268-z.
The effect of dietary cholesterol on the induction and development of colonic precursor lesions was determined in two mouse strains, C57BL/6J and BALB/cJ, which differ in their metabolism of cholesterol. Mice were randomized into four groups and fed a cholesterol-free or a 1.25% cholesterol diet during and/or subsequent to four weekly injections of azoxymethane (5 mg/kg body wt.). Dietary cholesterol significantly increased the number of aberrant crypt foci (P less than 0.0001), enhanced cell proliferation (P less than 0.0001) and induced alterations in the proliferative pattern and crypt morphometrics in the colonic epithelium of both mouse strains. While C57BL/6J mice developed a greater number of aberrant crypt foci than BALB/cJ mice (p less than 0.0001), a significant diet-strain interaction effect was not observed. The present results indicate that dietary cholesterol enhances the induction and development of chemically-induced colonic precancerous lesions but this process is not affected by genetic differences in cholesterol metabolism, as represented by the two strains of mice studied.
在两种胆固醇代谢存在差异的小鼠品系C57BL/6J和BALB/cJ中，测定了膳食胆固醇对结肠前体病变诱导和发展的影响。将小鼠随机分为四组，在每周注射一次偶氮甲烷（5毫克/千克体重），共注射四周期间和/或之后，给予无胆固醇饮食或1.25%胆固醇饮食。膳食胆固醇显著增加了异常隐窝灶的数量（P小于0.0001），增强了细胞增殖（P小于0.0001），并诱导了两种小鼠品系结肠上皮细胞增殖模式和隐窝形态计量学的改变。虽然C57BL/6J小鼠比BALB/cJ小鼠产生了更多的异常隐窝灶（P小于0.0001），但未观察到显著的饮食-品系交互作用效应。目前的结果表明，膳食胆固醇会增强化学诱导的结肠癌前病变的诱导和发展，但这一过程不受所研究的两种小鼠品系所代表的胆固醇代谢遗传差异的影响。
