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Changes of proton transportation across the inner mitochondrial membrane and H^+-ATPase in endotoxic shock rats 被引量:2

Changes of proton transportation across the inner mitochondrial membrane and H^+-ATPase in endotoxic shock rats
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摘要 Objective: To investigate the changes of proton transportation across the inner mitochondrial membrane (IMM) and H + ATPase of hepatocytes in endotoxic shock rats. Methods: Endotoxin from E.Coil of 5.0 mg/kg or saline of 1 ml/kg was injected into the femoral vein. The rats were sacrificed pre injection and 1, 3, 5, 8 hours after injection, and plasma and liver tissue samples were collected respectively. The liver tissue samples were used for preparation of mitochondria and submitochondrial particles (SMPs). The proton translocation of SMPs and H + ATPase, phospholipase A 2 (PLA 2) activities and malondialdehyde (MDA) content, membrane fluidities of different level of mitochondria membrane and plasma MDA content were assayed. Results: (1) Five hours after E. Coli. O111B4 injection, the maximum fluorescence quenching ACMA after adding ATP, nicotinamide adenin dinucleoacid hydrogen (NADH), and the succinate were significantly decreased (P< 0.05 ). The time of maximum fluorescent quenching and the half time of fluorescent quenching were significantly prolonged (P< 0.01 ), especially when NADH was used as a substrate. (2) The mitochondrial H + ATPase activity was significantly increased at early stage of endotoxic shock (P< 0.05 ), and significantly decreased at late stage of endotoxic shock (P< 0.01 ). (3) The mitochondrial membrane bound PLA 2 activity, plasmal and mitochondrial MDA content were significantly increased and succinate dehydrogenase (SDH) activity of mitochondria decreased markedly in endotoxic shock rats (P< 0.05 ). (4) The mitochondrial membrane fluidity of different lipid regions was decreased, especially in the head of phospholipid. Conclusions: Proton transportation across IMM and mitochondrial H + ATPase activity are significantly decreased in endotoxic shock.
出处 《Chinese Journal of Traumatology》 CAS 2003年第5期292-296,共5页 中华创伤杂志(英文版)
关键词 MITOCHONDRIA Shock septic H + ATPase 质子转运 线粒体膜 内毒素休克 动物模型 ATP酶 病理机制
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