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慢性酒精喂养后前列腺素类似物米索前列醇对大鼠肝线粒体的影响。

The effect of the prostaglandin analogue-misoprostol on rat liver mitochondria after chronic alcohol feeding.

作者信息

Dlugosz J W, Korsten M A, Lieber C S

机构信息

Alcohol Research and Treatment Center, Bronx VA Medical Center, NY 10468.

出版信息

Life Sci. 1991;49(13):969-78. doi: 10.1016/0024-3205(91)90080-u.

DOI:10.1016/0024-3205(91)90080-u
PMID:1909412
Abstract

Rats fed ethanol (36% of total calories in a nutritionally adequate liquid diet) for 5 weeks develop functional alterations of hepatic mitochondria and steatosis of the liver. At the fatty liver stage, ADP-stimulated respiration of mitochondria was depressed in ethanol fed rats by 30% (p less than 0.001) with glutamate + malate and by 23% (p less than 0.001) with succinate as substrates. A similar decrease was noted in the respiratory control ratio (RCR) (34% and 29%, respectively). The total lipid content of the liver increased 2.6 fold (p less than 0.001). Mitochondrial dysfunction could be prevented, in part, by the treatment with a synthetic derivative of prostaglandin E1, misoprostol, at a mean daily dose of 80 micrograms/kg of body weight. The RCR with glutamate + malate as substrates was improved by 36% (p less than 0.05). We conclude that misoprostol attenuates several functional alterations in liver mitochondria during alcohol feeding.

摘要

给大鼠喂食乙醇(占营养充足的液体饮食中总热量的36%)5周后,会出现肝线粒体功能改变和肝脏脂肪变性。在脂肪肝阶段,以谷氨酸 + 苹果酸为底物时,乙醇喂养的大鼠线粒体中ADP刺激的呼吸作用降低了30%(p < 0.001),以琥珀酸为底物时降低了23%(p < 0.001)。呼吸控制率(RCR)也有类似程度的下降(分别为34%和29%)。肝脏的总脂质含量增加了2.6倍(p < 0.001)。每天以平均80微克/千克体重的剂量用前列腺素E1的合成衍生物米索前列醇进行治疗,可部分预防线粒体功能障碍。以谷氨酸 + 苹果酸为底物时的RCR提高了36%(p < 0.05)。我们得出结论,米索前列醇可减轻酒精喂养期间肝脏线粒体的几种功能改变。

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引用本文的文献

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Effects of prostaglandins on ethanol damage in primary cultured rat hepatocytes.前列腺素对原代培养大鼠肝细胞乙醇损伤的影响。
Korean J Intern Med. 1998 Feb;13(1):1-9. doi: 10.3904/kjim.1998.13.1.1.
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Hepatic mitochondrial and lysosomal alterations in acute experimental pancreatitis with ethanolic coetiology in rats.乙醇性病因导致的大鼠急性实验性胰腺炎中肝脏线粒体和溶酶体的改变
Dig Dis Sci. 1996 Jan;41(1):139. doi: 10.1007/BF02208596.