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烧伤焦痂脂类组分D_1可抑制离体大鼠肝线粒体呼吸控制率(RCR)、ADP/O、第3态呼吸及ATP产生率,刺激第4态呼吸。预先加入维生素E(Vit.E)可非常显著地防止D_1对线粒体呼吸功能的抑制。后加Vit.E没有保护作用。D_1经热处理可非常显著地降低其对线粒体呼吸功能的抑制作用。氢过氧化枯烯(CHP)可非常显著地抑制线粒体呼吸功能。Vit.E可显著地防止较低浓度的CHP对线粒体RCR的抑制。还可使正常线粒体中以及加入D_1、HD_1和CHP,后线粒体中丙二醛含量显著减少。Vit.E为作用肯定的抗氧化剂,它的保护作用提示D_1和CHP极可能通过脂质过氧化作用这一共同途径损害线粒体功能。
Burn lipid component of estrogen D_1 can inhibit rat mitochondrial respiratory control rate (RCR), ADP / O, third state respiration and ATP production in vitro, and stimulate the fourth state respiration. Pre-addition of vitamin E (Vit.E) can very significantly prevent D_1 mitochondrial respiratory function inhibition. After adding Vit.E no protective effect. Heat treatment of D_1 significantly reduced its inhibitory effect on mitochondrial respiratory function. Cumene hydroperoxide (CHP) can very significantly inhibit mitochondrial respiratory function. Vit.E significantly prevented mitochondrial RCR inhibition by lower concentrations of CHP. But also significantly reduce the content of malondialdehyde in mitochondria and normal mitochondria, as well as D_1, HD_1 and CHP. Vit.E is an affirmative antioxidant and its protective effect suggests that Dl and CHP most likely impair mitochondrial function through a common pathway of lipid peroxidation.