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慢性乙醇处理对大鼠肝脏中叔丁基过氧化氢依赖性脂质过氧化的影响。

Effect of chronic ethanol treatment on the t-butyl hydroperoxide-dependent lipid peroxidation in rat liver.

作者信息

Antonenkov V D, Pirozhkov S V

机构信息

All-Union Research Center for Medico-Biological Problems of Narcology, Moscow, U.S.S.R.

出版信息

Int J Biochem. 1991;23(2):153-60. doi: 10.1016/0020-711x(91)90183-n.

Abstract
  1. The effect of chronic ethanol consumption on the level of the t-butyl hydroperoxide (Bu'OOH)-induced lipid peroxidation in rat liver homogenate and subcellular fractions was measured using chemiluminescence technique and malondialdehyde formation. 2. It was shown that under the action of ethanol the rate of lipid peroxidation was decreased in the whole and "postnuclear" liver homogenates. 3. Ethanol significantly decreased the intensity of lipid peroxidation in microsomes, but did not affect the Bu'OOH-dependent process in mitochondria. 4. The level of lipid peroxidation was reduced after incubation of the total particulate fraction (mitochondria plus microsomes) with the undialysed cytosol from ethanol-treated rat liver. Dialysis of the cytosol prevented depressive effect of ethanol treatment on lipid peroxidation. 5. Reduced glutathione (0.1-1.0 mM) was shown to decrease the rate of lipid peroxidation in rat liver microsomes, but did not affect its level in mitochondria. 6. Pyrazole injections to rats reduced and phenobarbital treatment increased the level of the Bu'OOH-dependent lipid peroxidation in liver microsomes. 7. The data obtained indicate that the Bu'OOH-dependent lipid peroxidation is not an appropriate marker of the ethanol-induced oxidative stress in rat liver cells.
摘要
  1. 采用化学发光技术和丙二醛生成法,测定了长期摄入乙醇对叔丁基过氧化氢(Bu'OOH)诱导的大鼠肝脏匀浆和亚细胞组分脂质过氧化水平的影响。2. 结果表明,在乙醇作用下,全肝和“核后”肝脏匀浆中的脂质过氧化速率降低。3. 乙醇显著降低了微粒体中脂质过氧化的强度,但不影响线粒体中依赖于Bu'OOH的过程。4. 用乙醇处理的大鼠肝脏未透析的细胞溶质孵育总微粒体组分(线粒体加微粒体)后,脂质过氧化水平降低。细胞溶质的透析可防止乙醇处理对脂质过氧化的抑制作用。5. 还原型谷胱甘肽(0.1 - 1.0 mM)可降低大鼠肝脏微粒体中脂质过氧化的速率,但不影响其在线粒体中的水平。6. 给大鼠注射吡唑可降低肝脏微粒体中依赖于Bu'OOH的脂质过氧化水平,而苯巴比妥处理则可增加该水平。7. 所得数据表明,依赖于Bu'OOH的脂质过氧化并非大鼠肝细胞乙醇诱导氧化应激的合适标志物。

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