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石油烃毒性机制:暴露于普拉德霍湾原油后大鼠肝脏线粒体的功能变化

Mechanisms of petroleum hydrocarbon toxicity: functional changes in rat liver mitochondria after exposure to a Prudhoe Bay Crude Oil.

作者信息

Khan S, Payne J F, Rahimtula A D

出版信息

Toxicol Lett. 1986 Jul-Aug;32(1-2):141-6. doi: 10.1016/0378-4274(86)90060-3.

DOI:10.1016/0378-4274(86)90060-3
PMID:3738925
Abstract

Administration of a Prudhoe Bay Crude Oil (PBCO) to rats (5 ml/kg/day for 2 days) resulted in a 30-35% inhibition of liver mitochondrial state 3 respiration with beta-hydroxybutyrate or succinate as substrates. beta-Hydroxybutyrate dehydrogenase, succinate dehydrogenase, NADH oxidase and succinate oxidase activities were also decreased in PBCO-treated rats. A significant increase in latent ATPase activity was also observed. Our results suggest that PBCO exerts its effects on liver mitochondria through the inhibition of beta-hydroxybutyrate- and succinate-supported electron transfer activities and by impairment of the mitochondrial membrane.

摘要

给大鼠注射普拉德霍湾原油(PBCO)(5毫升/千克/天,持续2天),以β-羟基丁酸酯或琥珀酸为底物时,肝脏线粒体状态3呼吸受到30 - 35%的抑制。在接受PBCO处理的大鼠中,β-羟基丁酸脱氢酶、琥珀酸脱氢酶、NADH氧化酶和琥珀酸氧化酶的活性也有所降低。还观察到潜在ATP酶活性显著增加。我们的结果表明,PBCO通过抑制β-羟基丁酸酯和琥珀酸支持的电子传递活性以及损害线粒体膜,对肝脏线粒体发挥作用。

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Mechanisms of petroleum hydrocarbon toxicity: functional changes in rat liver mitochondria after exposure to a Prudhoe Bay Crude Oil.石油烃毒性机制:暴露于普拉德霍湾原油后大鼠肝脏线粒体的功能变化
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