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柠檬酸亚铁诱导的线粒体氧化损伤会因钙离子而加剧,包括脂质过氧化和膜蛋白改变。

Oxidative damage of mitochondria induced by Fe(II)citrate is potentiated by Ca2+ and includes lipid peroxidation and alterations in membrane proteins.

作者信息

Castilho R F, Meinicke A R, Almeida A M, Hermes-Lima M, Vercesi A E

机构信息

Departamento de Bioquímica, Universidade Estadual de Campinas, SP, Brazil.

出版信息

Arch Biochem Biophys. 1994 Jan;308(1):158-63. doi: 10.1006/abbi.1994.1022.

Abstract

Isolated rat liver mitochondria exposed to Fe(II)citrate undergo lipid peroxidation and alterations in membrane proteins. These processes were associated with irreversible decrease in membrane potential and mitochondrial swelling. Lipid peroxidation was evidenced by the production of thiobarbituric acid-reactive substances and also by the reaction of these products with membrane proteins, through the formation of Schiff bases. Alterations in membrane proteins were also characterized by the loss of specific proteins that could be recovered from the mitochondrial supernatant as shown by SDS-polyacrylamide gel electrophoresis. The degree of both lipid peroxidation and alterations in membrane proteins were diminished by EGTA, ruthenium red, or dibucaine. This strongly indicates that Ca2+ potentiates the oxidative damage of mitochondria exposed to Fe(II)citrate.

摘要

暴露于柠檬酸亚铁的离体大鼠肝线粒体发生脂质过氧化和膜蛋白改变。这些过程与膜电位的不可逆降低和线粒体肿胀有关。脂质过氧化通过硫代巴比妥酸反应性物质的产生以及这些产物与膜蛋白通过席夫碱的形成反应来证明。膜蛋白的改变还表现为特定蛋白的丢失,如通过SDS-聚丙烯酰胺凝胶电泳所示,这些蛋白可从线粒体上清液中回收。EGTA、钌红或丁卡因可减轻脂质过氧化和膜蛋白改变的程度。这有力地表明Ca2+增强了暴露于柠檬酸亚铁的线粒体的氧化损伤。

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