Lii C K, Sung W C, Ko Y J, Chen H W
Department of Nutrition, Chung Shan Medical College, Taichung, Taiwan.
Nutr Cancer. 1998;32(1):37-42. doi: 10.1080/01635589809514714.
Hepatic cytochrome P-450 enzymes play important roles in bioactivation of chemical carcinogens, biotransformation of many endogenous compounds, and detoxification of numerous xenobiotics. These enzyme activities have been shown to be regulated by various dietary factors. In our previous study, hepatic cytochrome pentoxyresorufin O-dealkylase (PROD) activity was decreased in rats fed an alpha-tocopherol acetate-deficient diet compared with rats fed alpha-tocopherol acetate-adequate or -supplemented diets. The objective of the present study was to investigate whether the modulatory effect of dietary alpha-tocopherol acetate on hepatic cytochrome PROD activity is influenced by the presence of phenobarbital. Weanling male Sprague-Dawley rats were fed the AIN-76 diet for four days, fasted for two days, then fed semipurified diets that were alpha-tocopherol acetate deficient, adequate, or supplemented with 5 and 15 g/kg alpha-tocopherol acetate for four days. Liver and plasma alpha-tocopherol concentrations were dose dependently regulated by dietary alpha-tocopherol acetate level. Inhibition of lipid peroxidation by dietary alpha-tocopherol acetate was dose dependent. Hepatic total cytochrome P-450 content was significantly greater in rats fed diets supplemented with 5 and 15 g/kg alpha-tocopherol acetate than in rats fed an alpha-tocopherol-adequate diet (p < 0.05). Hepatic cytochrome PROD activity was significantly greater in rats fed diets supplemented with 5 and 15 g/kg alpha-tocopherol acetate than in rats fed alpha-tocopherol acetate-deficient and -adequate diets (p < 0.05). These results suggest that, in the presence of phenobarbital, dietary alpha-tocopherol acetate efficiently affects tissue alpha-tocopherol levels and inhibits lipid peroxidation and that diets supplemented with 5 or 15 g/kg alpha-tocopherol acetate enhance hepatic cytochrome PROD activity compared with alpha-tocopherol acetate-deficient or -adequate diets.
肝细胞色素P-450酶在化学致癌物的生物活化、许多内源性化合物的生物转化以及众多外源性物质的解毒过程中发挥着重要作用。这些酶的活性已被证明受多种饮食因素的调节。在我们之前的研究中，与喂食α-生育酚醋酸酯充足或补充饮食的大鼠相比，喂食α-生育酚醋酸酯缺乏饮食的大鼠肝细胞色素戊氧基试卤灵O-脱烷基酶（PROD）活性降低。本研究的目的是调查饮食中α-生育酚醋酸酯对肝细胞色素PROD活性的调节作用是否受苯巴比妥的影响。断乳雄性Sprague-Dawley大鼠先喂食AIN-76饮食四天，禁食两天，然后喂食α-生育酚醋酸酯缺乏、充足或补充5和15 g/kg α-生育酚醋酸酯的半纯化饮食四天。肝脏和血浆α-生育酚浓度受饮食中α-生育酚醋酸酯水平的剂量依赖性调节。饮食中α-生育酚醋酸酯对脂质过氧化的抑制作用呈剂量依赖性。喂食补充5和15 g/kg α-生育酚醋酸酯饮食的大鼠肝脏总细胞色素P-450含量显著高于喂食α-生育酚充足饮食的大鼠（p < 0.05）。喂食补充5和15 g/kg α-生育酚醋酸酯饮食的大鼠肝细胞色素PROD活性显著高于喂食α-生育酚醋酸酯缺乏和充足饮食的大鼠（p < 0.05）。这些结果表明，在存在苯巴比妥的情况下，饮食中的α-生育酚醋酸酯有效地影响组织α-生育酚水平并抑制脂质过氧化，并且与α-生育酚醋酸酯缺乏或充足饮食相比，补充5或15 g/kg α-生育酚醋酸酯的饮食可增强肝细胞色素PROD活性。
