Mitochondrial hydrogen peroxide generation and activities of glutathione peroxidase and superoxide dismutase following global ischemia.
Mitochondrial hydrogen peroxide generation and activities of glutathione peroxidase and superoxide dismutase following global ischemia.
复制标题
整体缺血后线粒体过氧化氢的产生以及谷胱甘肽过氧化物酶和超氧化物歧化酶的活性。
DOI：
10.1016/s0022-2828(87)80530-8
复制
发表时间：
1987
影响因子：
5
通讯作者：
Adkins,S
中科院分区：
文献类型：
--
作者：
Shlafer,M;Myers,CL;Adkins,S
我们使用分离的、缓冲灌注的兔心脏来评估全面、常温缺血是否改变线粒体过氧化氢（H2O2）的产生和线粒体中降解H2O2和超氧阴离子（O2）的主要酶的活性。−)分别为谷胱甘肽过氧化物酶（GPD）和超氧化物歧化酶（SOD）。该制剂缺乏外源性中性粒细胞和内源性黄嘌呤氧化酶，这是氧代谢产物的其他潜在来源。缺血抑制线粒体氧化磷酸化参数、State 4琥珀酸支持的h2o2生成速率以及State 4耗氧量转化为h2o2生成的相对通量。h2o2的生产并没有停止。缺血和再灌注显著降低线粒体部分SOD（43%）和GPD（39%）的活性。胞浆GPD活性也下降。结果表明，心肌细胞的酶降解h2o2和O2的能力。−受到损害，特别是在线粒体中。虽然线粒体h2o2的产生减少，但线粒体可能在缺血后继续作为这种氧代谢物的来源。总的来说，这些数据可能有助于解释为什么线粒体是自由基介导的缺血损伤的脆弱目标。
We used isolated,buffer-perfused rabbit hearts to evaluate whether global, normothermic ischemia altered mitochondrial hydrogen peroxide (H2O2) generation and mitochondrial activities of the major enzymes responsible for degrading H2O2and superoxide anion (O2.−): glutathione peroxidase (GPD) and superoxide dismutase (SOD), respectively. This preparation lacks exogenous neutrophils and endogenous xanthine oxidase, which are other potential sources of oxygen metabolites. Ischemia depressed mitochondrial oxidative phosphorylation parameters, State 4 succinate-supported H2O2generation rates, and the relative flux of State 4 oxygen consumption that was diverted to H2O2formation. The production of H2O2was not abolished. Ischemia and reperfusion significantly reduced the activities of SOD (by 43%) and GPD (by 39%) in the mitochondrial fraction. Cytosolic GPD activity was also depressed.The results suggest that the myocardial cell's ability to enzymatically degrade H2O2and O2.−is compromised,particularly in the mitochondrion. Although mitochondrial H2O2production is decreased, the mitochondria may persist as a source of this oxygen metabolite following ischemia. Collectively, the data may help explain why mitochondria are vulnerable targets of free radical-mediated damage due to ischemia.