Effect of dietary ethanol and cholesterol on metabolic functions of hepatic mitochondria and microsomes from the monkey, Macaca nemestrina.
Effect of dietary ethanol and cholesterol on metabolic functions of hepatic mitochondria and microsomes from the monkey, Macaca nemestrina.
复制标题
膳食乙醇和胆固醇对猕猴肝线粒体和微粒体代谢功能的影响。
DOI：
10.1111/j.1530-0277.1981.tb04924.x
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Leathers,C
中科院分区：
文献类型：
--
作者：
Cunningham,CC;Sinthusek,G;Spach,PI;Leathers,C
猴子（Macaca nemestrina）被分成四组，每组都喂食特定的饮食。饮食中的变量如下：饮食A，0.3 mg胆固醇/kcal营养素;饮食B，1.0 mg胆固醇/kcal营养素;饮食C，0.3 mg胆固醇/kcal营养素，乙醇（36%的卡路里）;饮食D，1.0 mg胆固醇/ kcal营养素，乙醇（36%的卡路里）。食用含有乙醇的食物的猴子患上了脂肪肝。来自乙醇喂养动物的线粒体显示解偶联剂刺激的状态3和状态4琥珀酸氧化活性显著降低;呼吸控制率;和ATP含量。从乙醇喂养组分离的肝微粒体显示出以NADPH或H2 O2作为共底物时乙醇氧化活性增加。乙醇喂养动物的苯胺羟化酶和氨基比林-N-脱甲基酶活性也升高。这些功能特性的改变主要与饮食中的乙醇有关。虽然胆固醇的干扰作用小于乙醇，但确实引起线粒体细胞色素氧化酶活性显著降低，微粒体相关乙醇氧化活性小幅但具有统计学显著性增加。它似乎增强了乙醇降低线粒体呼吸控制和ATP浓度的作用。
Monkeys(Macaca nemestrina)were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, i.O mg cholesterol/ kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria from ethanol‐fed animals demonstrated significant decreases in uncoupler‐stimulated, state 3, and state 4 succinate oxidation activity; respiratory control ratio; and ATP content. Liver microsomes isolated from the ethanol‐fed groups demonstrated increased ethanol oxidizing activity with either NADPH or H2O2 as cosubstrate. Aniline hydroxylase and ami‐nopyrine‐N‐demethylase activities were also elevated in ethanol‐fed animals. The alterations in these functional properties were related primarily to ethanol in the diets. Cholesterol, while being less of a perturbant than ethanol, did elicit a significant decrease in cytochrome oxidase activity of mitochondria and a small but statistically significant increase in microsomal‐associated ethanol oxidation activity. It appeared to potentiate the effect of ethanol in lowering mitochondrial respiratory control and ATP concentrations.