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乙醇诱导的大鼠肾脏氧化还原失衡。

Ethanol-induced redox imbalance in rat kidneys.

机构信息

Department of Animal Biology, Faculty of Biology, University of Bucharest, 050095 Bucharest, Romania.

出版信息

J Biochem Mol Toxicol. 2011 Jul-Aug;25(4):224-30. doi: 10.1002/jbt.20379. Epub 2010 Nov 23.

DOI:10.1002/jbt.20379
PMID:21812072
Abstract

This study reports the effects of long-term ethanol consumption on kidney redox status, in terms of enzymatic mechanisms involved in regulating the cytosolic [NADH]/[NAD(+) ] balance. Wistar rats were treated with ethanol (2 g/kg body weight/24 h) via intragastric intubation for 10 and 30 weeks, respectively. Ethanol administration induced an enhancement of alcohol dehydrogenase activities and affected the capacity of the kidney to prevent NADH accumulation in the cytosol. After 10 weeks, the excess of NADH was balanced by increased activities of malate dehydrogenase and aspartate transaminase. In the event of a longer period of ethanol intake, the kidney was not able to balance the NADH excess, even though an increase in malate dehydrogenase, lactate dehydrogenase, aspartate transaminase, and alanine transaminase activities was noted. The electrophoretic analysis of alcohol dehydrogenase, lactate dehydrogenase, and malate dehydrogenase isoforms revealed differences between control and ethanol-treated animals. The results suggest that rat kidneys have a multicomponent metabolic response to the same daily dose of ethanol that functions to maintain the redox status and which varies with the length of the administration period.

摘要

本研究报告了长期乙醇摄入对肾脏氧化还原状态的影响,具体表现在参与调节细胞溶胶 [NADH]/[NAD(+) ]平衡的酶机制方面。Wistar 大鼠通过胃内插管分别给予乙醇(2 g/kg 体重/24 h)10 和 30 周。乙醇给药诱导了醇脱氢酶活性的增强,并影响了肾脏防止细胞溶胶中 NADH 积累的能力。10 周后,通过增加苹果酸脱氢酶和天冬氨酸转氨酶的活性来平衡 NADH 的过剩。在更长时间的乙醇摄入情况下,肾脏即使增加了苹果酸脱氢酶、乳酸脱氢酶、天冬氨酸转氨酶和丙氨酸转氨酶的活性,也无法平衡 NADH 的过剩。电泳分析显示,乙醇处理组和对照组的醇脱氢酶、乳酸脱氢酶和苹果酸脱氢酶同工酶存在差异。结果表明,大鼠肾脏对相同的每日乙醇剂量有多种代谢反应,这些反应有助于维持氧化还原状态,且随着给药时间的延长而变化。

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Ethanol-induced redox imbalance in rat kidneys.乙醇诱导的大鼠肾脏氧化还原失衡。
J Biochem Mol Toxicol. 2011 Jul-Aug;25(4):224-30. doi: 10.1002/jbt.20379. Epub 2010 Nov 23.
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