Madesh M, Balasubramanian K A
Department of Gastrointestinal Sciences, Christian Medical College Hospital, Vellore, India.
Arch Biochem Biophys. 1997 Oct 15;346(2):187-92. doi: 10.1006/abbi.1997.0288.
Mitochondrial damage is one of the prominent features of cell injury during oxidative stress and altered mitochondrial lipids may contribute to this damage. Lipid changes were observed when liver mitochondria were exposed to superoxide generating systems. Phosphatidylcholine and phosphatidylethanolamine contents were decreased with simultaneous formation of lysophospholipids when exposed to superoxide. Among the neutral lipids there was an increase in the level of free fatty acids. This alteration in lipid composition could be prevented by the simultaneous presence of superoxide dismutase or phospholipase A2 (PLA2) inhibitors. H2O2 did not have any effect on liver mitochondrial PLA2. This suggests that superoxide anion stimulates phospholipase A2 which is prevented by superoxide scavenging agents and PLA2 inhibitors. The products of phospholipase A2 are membrane-damaging agents which may be responsible for mitochondrial damage seen during oxidative stress.
线粒体损伤是氧化应激期间细胞损伤的突出特征之一，线粒体脂质改变可能导致这种损伤。当肝线粒体暴露于超氧化物生成系统时，观察到脂质变化。暴露于超氧化物时，磷脂酰胆碱和磷脂酰乙醇胺含量降低，同时溶血磷脂形成。在中性脂质中，游离脂肪酸水平升高。脂质组成的这种改变可通过同时存在超氧化物歧化酶或磷脂酶A2（PLA2）抑制剂来预防。H2O2对肝线粒体PLA2没有任何影响。这表明超氧阴离子刺激磷脂酶A2，而超氧化物清除剂和PLA2抑制剂可阻止这种刺激。磷脂酶A2的产物是膜损伤剂，可能是氧化应激期间所见线粒体损伤的原因。
