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氯化镧和氯化钕处理下雏鸡肝脏线粒体的抗氧化保护机制

Antioxidant protection mechanism of chick hepatic mitochondria exposed to lanthanum chloride & neodymium chloride treatment.

作者信息

Ghosh N, Chattopadhyay D, Chatterjee G C

机构信息

Department of Biochemistry, University College of Science, Calcutta, India.

出版信息

Indian J Exp Biol. 1991 May;29(5):486-8.

PMID:1916948
Abstract

Acute lanthanum chloride (250 mg/kg body wt) and neodymium chloride (200 mg/kg body wt) administrations resulted in significant enhancement of glutathione level in chick hepatic mitochondria. However, glutathione-s-transferase activity was depressed. There was no alteration in the activity of glutathione reductase. Activity of glucose-6-phosphate dehydrogenase was not altered under lanthanum and neodymium treatment. There was a significant enhancement of intramitochondrial glutathione peroxidase and superoxide dismutase. Lipid peroxidation remains the same as control group of animals.

摘要

急性给予氯化镧(250毫克/千克体重)和氯化钕(200毫克/千克体重)可显著提高雏鸡肝脏线粒体中的谷胱甘肽水平。然而,谷胱甘肽-S-转移酶的活性受到抑制。谷胱甘肽还原酶的活性没有变化。在镧和钕处理下,葡萄糖-6-磷酸脱氢酶的活性未改变。线粒体内谷胱甘肽过氧化物酶和超氧化物歧化酶显著增强。脂质过氧化与动物对照组保持相同。

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