OXIDATIVE DAMAGE OF MITOCHONDRIA INDUCED BY FE(II)CITRATE IS POTENTIATED BY CA2+ AND INCLUDES LIPID-PEROXIDATION AND ALTERATIONS IN MEMBRANE-PROTEINS
OXIDATIVE DAMAGE OF MITOCHONDRIA INDUCED BY FE(II)CITRATE IS POTENTIATED BY CA2+ AND INCLUDES LIPID-PEROXIDATION AND ALTERATIONS IN MEMBRANE-PROTEINS
复制标题
DOI：
10.1006/abbi.1994.1022
复制
发表时间：
1994-01-01
影响因子：
3.9
通讯作者：
VERCESI, AE
中科院分区：
文献类型：
--
作者：
CASTILHO, RF;MEINICKE, AR;VERCESI, AE
分离的大鼠肝线粒体暴露于柠檬酸铁后会发生脂质过氧化和膜蛋白的改变。这些过程与膜电位不可逆转的降低和线粒体肿胀有关。脂质过氧化的证据是硫代巴比妥酸反应物质的产生，以及这些产物通过形成席夫碱与膜蛋白的反应。膜蛋白的改变也表现为线粒体上清液中可回收的特定蛋白的丢失，如SDS-聚丙烯酰胺凝胶电泳法所示。EGTA、Ru红或地布卡因均可减轻脂质过氧化程度和膜蛋白的改变。这有力地表明，Ca~(2+)加重了柠檬酸铁暴露下线粒体的氧化损伤。
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.