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首页> 外文期刊>Life sciences >Oxidative damage of rat liver mitochondria during exposure to t-butyl hydroperoxide. Role of Ca2 + ions in oxidative processes
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Oxidative damage of rat liver mitochondria during exposure to t-butyl hydroperoxide. Role of Ca2 + ions in oxidative processes

机译：暴露于叔丁基氢过氧化物期间大鼠肝线粒体的氧化损伤。 Ca2 +离子在氧化过程中的作用

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Aims The present study was designed for further evaluation of the biochemical mechanism of hepatic mitochondrial dysfunction under oxidative damages induced by organic hydroperoxide, tert-butyl hydroperoxide (tBHP), for estimation of the molecular targets impaired during oxidative stress, and for investigation of the role of Ca2 + ions in mitochondrial oxidative reactions and of the protective effect of melatonin during mitochondrial peroxidative damage. Main methods Mitochondria were isolated by differential centrifugation from the rat liver. The effects of tBHP exposure, EDTA, Ca 2 + ions and melatonin on mitochondrial respiratory activity, mitochondrial enzyme activities and redox status were measured. Key findings The present study provides evidence that tBHP (at low concentrations of 0.02-0.065 mM, in EDTA-free medium) induced uncoupling of the oxidation and phosphorylation processes and decreased the efficiency of the phosphorylation reaction. This effect depended on the respiratory substrate used. The presence of EDTA prevented oxidative impairment of mitochondrial respiration, but Ca 2 + ions in the medium enhanced oxidant-induced mitochondrial damage considerably. In the presence of 0.5 mM EDTA, tBHP (at high concentrations, 0.5-2 mM) considerably oxidized mitochondrial reduced glutathione, enhanced accumulation of membrane lipid peroxidation products and mixed protein-glutathione disulfides and led to an inhibition of oxoglutarate dehydrogenase and succinate dehydrogenase. Significance Direct oxidative modification of enzymatic complexes of the respiratory chain and mitochondrial matrix, mitochondrial reduced glutathione depletion, protein glutathionylation, membrane lipid peroxidation and Ca2 + overload are the main events of mitochondrial peroxidative damages. Experiments in vitro demonstrated that melatonin inhibited the mitochondrial peroxidative damage, preventing redox-balance changes and succinate dehydrogenase inactivation.
机译：目的本研究旨在进一步评估在有机过氧化氢，叔丁基过氧化氢（tBHP）引起的氧化损伤下肝线粒体功能障碍的生化机制，用于估计氧化应激期间受损的分子靶标，并研究其作用。离子在线粒体氧化反应中的作用以及褪黑素在线粒体过氧化损伤中的保护作用。主要方法通过差速离心从大鼠肝脏中分离线粒体。测量了tBHP暴露，EDTA，Ca 2+离子和褪黑激素对线粒体呼吸活性，线粒体酶活性和氧化还原状态的影响。关键发现本研究提供的证据表明，tBHP（低浓度0.02-0.065 mM，在无EDTA的培养基中）引起氧化和磷酸化过程的解偶联，并降低了磷酸化反应的效率。该效果取决于所用的呼吸基质。 EDTA的存在阻止了线粒体呼吸的氧化损伤，但是培养基中的Ca 2+离子大大增强了氧化剂引起的线粒体损伤。在存在0.5 mM EDTA的情况下，tBHP（在高浓度下为0.5-2 mM）大大氧化了线粒体，减少了谷胱甘肽，增强了膜脂质过氧化产物和蛋白质-谷胱甘肽二硫化物混合的积累，并导致了对氧谷氨酸脱氢酶和琥珀酸脱氢酶的抑制。意义呼吸链和线粒体基质酶复合物的直接氧化修饰，线粒体减少的谷胱甘肽耗竭，蛋白质谷胱甘肽酰化，膜脂质过氧化和Ca2 +超载是线粒体过氧化损伤的主要事件。体外实验证明褪黑素可抑制线粒体的过氧化损伤，从而防止氧化还原平衡变化和琥珀酸脱氢酶失活。

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