Snodgrass P J
Veterans Administration Medical Center, Indianapolis, Indiana 46202.
Hepatology. 1989 Mar;9(3):373-9. doi: 10.1002/hep.1840090306.
We produced moderately severe, inactive micronodular cirrhosis in rats using CCl4 and measured the urea cycle enzyme activities in liver after feeding a 15% casein diet for 1 week and again after a 60% casein diet for 1 week. There was no deficiency of any of the five urea cycle enzymes in cirrhotic livers of rats pair-fed the 15% casein diet. Argininosuccinate synthetase and carbamyl phosphate synthetase activities were lower than in non-pair-fed controls by some baselines. All five enzymes in cirrhotic livers were induced 1.5- to 3-fold by the high-protein diet expressed as units per 100 gm of rat. The level of carbamyl phosphate synthetase activity was lower in the livers of rats pair-fed the 60% casein diet than in control livers based on wet weight, collagen-free protein and DNA, but the activities were equal expressed as units per 100 gm of rat. This example of CCl4-induced cirrhosis in the rat does not serve as a good model for human cirrhosis, in which the urea cycle enzymes are reported to be decreased in activity.
我们使用四氯化碳在大鼠中制造了中度严重的非活动性微结节性肝硬化，并在给予15%酪蛋白饮食1周后以及再次给予60%酪蛋白饮食1周后测量了肝脏中的尿素循环酶活性。在配对喂食15%酪蛋白饮食的大鼠肝硬化肝脏中，五种尿素循环酶均无缺乏。精氨琥珀酸合成酶和氨甲酰磷酸合成酶的活性比未配对喂食的对照组低一些基线水平。以每100克大鼠为单位表示，高蛋白饮食可使肝硬化肝脏中的所有五种酶诱导1.5至3倍。基于湿重、无胶原蛋白蛋白和DNA，配对喂食60%酪蛋白饮食的大鼠肝脏中氨甲酰磷酸合成酶活性水平低于对照肝脏，但以每100克大鼠为单位表示时，活性相等。大鼠中这种四氯化碳诱导的肝硬化实例不能作为人类肝硬化的良好模型，据报道人类肝硬化中尿素循环酶的活性会降低。
