| Abstract: | （1）自由基所誘發的脂質過氧化作用，造成動物體內細胞傷害，而維生素Ｅ主要存在細胞膜上，是目前已知最重要的天然脂溶性抗氧化劑，它可以藉由本身結構中的酚基，提供一個氫質子轉移到自由基，而達到抗氧化的防禦作用。近年來也有研究指出，維生素Ｅ的攝取對於老鼠肝臟微粒體氧化原代謝酵素會產生影響，所以本次實驗有兩大目標，一是探討飲食中維生素Ｅ對於動物體內抗氧化系統的影響，二是評估它對肝臟微粒體酵素系統的影響。
實驗採用18隻雄性 Sprague-Dawley大鼠，分成三組分別餵飼含0、100和1500ppm維生素Ｅ的飼料七週，實驗分析項目，在抗氧化系統方面比較三組老鼠紅血球、血漿和肝臟組織脂質過氧化物濃度（TBARS），維生素Ｃ、Ｅ含量，麩胱甘月太（GSH），GSSG，尿酸（uricacid）濃度，以及麩胱甘月太還原酉每（GSH reductase），麩胱甘月太過氧化酉每（GSH peroxidase）以及超氧化歧化酉每（SOD）活性；肝臟微粒體酵系統分析 total p450 content, NADPH P450 reductase、CYＰ2EI、CYP2B1及GST活性。
結果顯示飼料中維生素Ｅ顯著影響血漿及肝臟中維生素Ｅ的濃度，而且維生素Ｅ能有效的抑制TBARS的形成。在抗氧化作用方面顯示維生素Ｅ對紅血球GSH、GSSG、肝臟細胞質部分的SOD和GSH reductase活性及血漿中 uric acid 濃度有顯著影響。而對微粒體酵素系統方面 CYP2B1和GST酵素活性，會隨維生素Ｅ含量增加而有增加趨的勢。
（2）肝臟中細胞色素 P-450在致癌物的生物活化、內生性物質的生物轉換及毒物的解毒作用扮演重要的角色，然而這些酵素活性會受到不同飲食因子所調控，最近的研究報告指出，餵飼不同含量維生素Ｅ，會影響大鼠肝中CYP2B1活性。
實驗採用16隻雄性 Sporague-Dawley 大鼠，餵飼AIN-76diet四天，接著空腹兩天，之後大鼠分成四組分別餵飼含0、100、5000 和15000ppm 維生素Ｅ飲食四天，大鼠犧牲前連續給與腹腔注射 phenobarbital（75mg/kg）三天，以誘發細胞色素 p450 2B1活性。
結果顯示經過phenobarbital腹腔注射的大鼠，飼料中維生素Ｅ含量顯著影響血漿及肝臟組織中維生素Ｅ濃度，並且維生素Ｅ能有效地抑制TBARS的產生。至於在解毒酵素方面，CYP2B1活性在餵飼5000和15000ppm維生素Ｅ的大鼠相較於餵飼100及0ppm維生素Ｅ的大鼠，活性有明顯提升（p<0.05）；餵飼5000及15000ppm維生素Ｅ的大鼠，細胞色素P450含量顯著高於餵飼100ppm維生素Ｅ之大鼠（p< 0.05）。
由此實驗結果得知，飲食中維生素Ｅ的添加確實會影響phenobarbitsl誘發解毒酵素CYP2B1。
(1)Lipid peroxidation caused by free-radicals leads to destruction of cells in the animal body. Vitamin E present mainly in the cell membrane, is recognized as one of the most important natural fat-soluble antioxidant, With the premence of phenyl group can transfer a hydrogen atom to the free radical, thereby exerts its antioxidative effect. Recent researches have shown that dietary vitamin E can affects the activities of hepatic cytochrome P-450 enzymes , however the results were not consistent. The goals of the present study are to investigate the influence of vitamin E on antioxidant status and antioxidant emzymes and to investigate the effect of vitamin E on activities of hepatic cytochrome P-450 enzymes. Three groups of 6 Sprague-Dawley rats were fed 0,100 or 1500 ppm vitamin E for 7weeks. The results show that dietary vitamin E significantly influence the concentrations of vitamin E in plasma and liver, and vitamin E can significanltly inhibit the formation of TBARS (p<0.05) . For antioxidative effect, is show that vitamin E affects the concentrations of RBC reduced glutathione (GSH),and GSSG, SOD and GSH reductase activities in hepatic cytosolic fraction, and uric acid level in the plasma. For microsomal enzymes, the CYR2B1 and GST activities were positively correlated with the dietary vitamin E level.
(2)Hepatic cytochrome P-450 enzymes play important roles in the bioactivation of chenmical carinogens, the biotransformation of many endogenous compounds, and the detoxification of numerous xenobiotics. These eczyme activities have been showed to be regulated by various dietary factors. The objective of the present study was to investigate the effect of dietary vitamin E on hepatic cytochrome P-450 2B1 activity in the presence of phenoberbital. Weaning male Sprague-Dawley rats were fed the AIN-76 diet for 4 days, then fasted 2 days, followed by semipurified diets containing 0,100,5000 or 15000ppm vitamin E for 4 days, Both liver and plasma □-tocopherol concentrations were dose-dependently regulated by dietary vitamin E level. The inhibition of lipid peroxidation by dietary vitamin E was dose-dependent. Rats fed diets containing 5000 and 15000 ppm vitamin E and significantly greater hepatic total cytochrome P-450 content than rats fed diets containing 100ppm vitamin E (p<0.05).Hepatic cytochrome P-450 2B1 activity was significantly greater in rats fed diets containing 5000 and 15000 ppm vitamin E than in rats fed diets containing 0 or 100 ppm vitamin E(p<0.05), these results suggest that ,in the presence of phenobarbital induction, dietary vitamin E efficiently affects tissue □- tocopherol level and inhibits lipid peroxidation, and that vitamin E supplementation (a diet containing5000 or 15000 ppm) enhances hepatic cytochrome P-450 2B1 activity compared to a diet containing 0 or 100 ppm vitamin E. |
