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[急性缺氧及缺氧-高氧适应状态下的线粒体硫醇-二硫键系统]

[Mitochondrial thiol-disulfide system under acute hypoxia and hypoxic-hyperoxic adaptation].

作者信息

Honchar O O, Man'kovs'ka I M

出版信息

Ukr Biochem J. 2014 Jan-Feb;86(1):93-100.

Abstract

The authors investigated the state of mitochondrial glutathione pool (reduced and oxidized glutathione, protein-GSH mixed disulfides), content of carbonyl groups and free sulfhydryl groups of proteins, protein expression of key mitochondrial antioxidant enzymes such as glutathione peroxidase and thioredoxin reductase as well as activity of glutathione reductase, glutathione peroxidase and glutaredoxin in the liver mitochondria of rats exposed to acute hypoxia after prolonged hypoxic-hyperoxic training (HHT). It was shown that the preliminary HHT reduced the intensity of proteins oxidative modification under acute hypoxia, activated the mitochondrial antioxidant defense as well as affected the thiol-disulfide exchange, redox balance in mitochondria, modulated the S-glutathionylation/deglutathionylation process in mitochondria membranes.

摘要

作者研究了长时间低氧-高氧训练(HHT)后暴露于急性低氧的大鼠肝脏线粒体中谷胱甘肽池的状态(还原型和氧化型谷胱甘肽、蛋白质-谷胱甘肽混合二硫化物)、蛋白质羰基和游离巯基的含量、关键线粒体抗氧化酶如谷胱甘肽过氧化物酶和硫氧还蛋白还原酶的蛋白质表达以及谷胱甘肽还原酶、谷胱甘肽过氧化物酶和谷氧还蛋白的活性。结果表明,预先进行的HHT降低了急性低氧条件下蛋白质氧化修饰的强度,激活了线粒体抗氧化防御,影响了线粒体中的硫醇-二硫化物交换、氧化还原平衡,调节了线粒体膜中的S-谷胱甘肽化/去谷胱甘肽化过程。

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