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酒精引起的肝脏线粒体变化。

Alcohol-induced mitochondrial changes in the liver.

作者信息

Gordon E R

出版信息

Recent Dev Alcohol. 1984;2:143-58. doi: 10.1007/978-1-4684-4661-6_9.

DOI:10.1007/978-1-4684-4661-6_9
PMID:6729159
Abstract

The chronic ingestion of ethanol results in liver-cell damage, and characteristic features of this injury are the marked alterations in both the functions and morphology of the mitochondria. Morphologically, the changes observed in human alcoholics and experimental animals appear similar. Bizarrely shaped mitochondria and megamitochondria are detected at the fatty liver stage and persist as the disease progresses. As yet, however, no correlation has been found between the severity of these morphological changes and the development of cirrhosis. Analysis of the mitochondrial membranes indicates that ethanol consumption produces changes in both the protein and lipid composition of the membrane. Profound decreases in the components of the respiratory chain have been detected, and these changes are associated with marked depressions in the activity of NAD+-linked dehydrogenases, cytochrome oxidase, and the ATP synthetase complex. On the other hand, no consistent pattern has emerged as to the effect of chronic ethanol consumption on the composition of the membrane phospholipids. Many of the changes appear to be dependent on the sex of the animal, the dietary status, and the duration of ethanol intake, and are suggestive of changes in fatty acid desaturase activity. Mitochondria isolated from ethanol-fed rats displayed impaired respiration and a lowered steady-state rate of ATP synthesis. Whether or not these functional changes are directly related to alterations in the physical properties of the membranes remains to be resolved. This marked depression of respiratory functions in isolated mitochondria was not reflected by a significant decrease in O2 consumption by the livers of ethanol-fed animals.

摘要

长期摄入乙醇会导致肝细胞损伤,这种损伤的特征性表现是线粒体的功能和形态均发生显著改变。从形态学上看,在人类酗酒者和实验动物身上观察到的变化相似。在脂肪肝阶段可检测到形状怪异的线粒体和巨型线粒体,且随着疾病进展持续存在。然而,目前尚未发现这些形态学变化的严重程度与肝硬化的发展之间存在关联。对线粒体膜的分析表明,乙醇摄入会导致膜的蛋白质和脂质组成发生变化。已检测到呼吸链成分显著减少,这些变化与NAD⁺连接的脱氢酶、细胞色素氧化酶和ATP合成酶复合体的活性显著降低有关。另一方面,关于长期摄入乙醇对膜磷脂组成的影响,尚未出现一致的模式。许多变化似乎取决于动物的性别、饮食状况以及乙醇摄入的持续时间,提示脂肪酸去饱和酶活性发生了变化。从喂食乙醇的大鼠中分离出的线粒体显示呼吸功能受损,ATP合成的稳态速率降低。这些功能变化是否与膜的物理性质改变直接相关仍有待解决。在分离的线粒体中呼吸功能的显著降低,并未在喂食乙醇的动物肝脏的氧气消耗显著减少中得到体现。

相似文献

1
Alcohol-induced mitochondrial changes in the liver.酒精引起的肝脏线粒体变化。
Recent Dev Alcohol. 1984;2:143-58. doi: 10.1007/978-1-4684-4661-6_9.
2
Biochemical and morphological alterations of baboon hepatic mitochondria after chronic ethanol consumption.慢性乙醇摄入后狒狒肝脏线粒体的生化和形态学改变。
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Alcohol, protein metabolism, and liver injury.酒精、蛋白质代谢与肝损伤。
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Decreased cytochrome oxidase activity in hepatic mitochondria after chronic ethanol consumption and the possible role of decreased cytochrome aa3 content and changes in phospholipids.长期乙醇摄入后肝线粒体细胞色素氧化酶活性降低以及细胞色素aa3含量降低和磷脂变化的可能作用。
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Membranes and phospholipids of liver mitochondria from chronic alcoholic rats are resistant to membrane disordering by alcohol.慢性酒精中毒大鼠肝脏线粒体的膜和磷脂对酒精引起的膜紊乱具有抗性。
Proc Natl Acad Sci U S A. 1981 Apr;78(4):2582-6. doi: 10.1073/pnas.78.4.2582.
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The methyl donor S-adenosylmethionine prevents liver hypoxia and dysregulation of mitochondrial bioenergetic function in a rat model of alcohol-induced fatty liver disease.甲基供体S-腺苷甲硫氨酸可预防酒精性脂肪性肝病大鼠模型中的肝脏缺氧及线粒体生物能量功能失调。
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Comparative effects of chronic ethanol consumption on the properties of mitochondria from rat brain and liver.
Alcohol Clin Exp Res. 1992 Feb;16(1):1-4. doi: 10.1111/j.1530-0277.1992.tb00625.x.

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