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泛醇-6的自氧化不依赖于超氧化物歧化酶。

Autoxidation of ubiquinol-6 is independent of superoxide dismutase.

作者信息

Schultz J R, Ellerby L M, Gralla E B, Valentine J S, Clarke C F

机构信息

Department of Chemistry and Biochemistry, University of California, Los Angeles 90095-1569, USA.

出版信息

Biochemistry. 1996 May 28;35(21):6595-603. doi: 10.1021/bi960245h.

DOI:10.1021/bi960245h
PMID:8639607
Abstract

Ubiquinone (Q) is an essential, lipid soluble, redox component of the mitochondrial respiratory chain. Much evidence suggests that ubiquinol (QH2) functions as an effective antioxidant in a number of membrane and biological systems by preventing peroxidative damage to lipids. It has been proposed that superoxide dismutase (SOD) may protect QH2 form autoxidation by acting either directly as a superoxide-semiquinone oxidoreductase or indirectly by scavenging superoxide. In this study, such an interaction between QH2 and SOD was tested by monitoring the fluorescence of cis-parinaric acid (cPN) incorporated phosphatidylcholine (PC) liposomes. Q6H2 was found to prevent both fluorescence decay and generation of lipid peroxides (LOOH) when peroxidation was initiated by the lipid-soluble azo initiator DAMP, dimethyl 2,2'-azobis (2-methylpropionate), while Q6 or SOD alone had no inhibitory effect. Addition of either SOD or catalase to Q6H2-containing liposomes had little effect on the rate of peroxidation even when incubated in 100% O2. Hence, the autoxidation of QH2 is a competing reaction that reduces the effectiveness of QH2 as an antioxidant and was not slowed by either SOD or catalase. The in vivo interaction of SOD and QH2 was also tested by employing yeast mutant strains harboring deletions in either CuZnSOD and/or MnSOD. The sod mutant yeast strains contained the same percent Q6H2 per cell as wild-type cells. These results indicate that the autoxidation of QH2 is independent of SOD.

摘要

泛醌(Q)是线粒体呼吸链中一种必需的、脂溶性的氧化还原成分。大量证据表明,泛醇(QH2)通过防止脂质的过氧化损伤,在许多膜和生物系统中作为一种有效的抗氧化剂发挥作用。有人提出,超氧化物歧化酶(SOD)可能通过直接作为超氧化物 - 半醌氧化还原酶或通过清除超氧化物间接作用来保护QH2免受自氧化。在本研究中,通过监测掺入顺式 - 紫黄质酸(cPN)的磷脂酰胆碱(PC)脂质体的荧光来测试QH2与SOD之间的这种相互作用。当由脂溶性偶氮引发剂DAMP(2,2'-偶氮二(2 - 甲基丙酸)二甲酯)引发过氧化时,发现Q6H2可防止荧光衰减和脂质过氧化物(LOOH)的产生,而单独的Q6或SOD没有抑制作用。即使在100%氧气中孵育,向含Q6H2的脂质体中添加SOD或过氧化氢酶对过氧化速率的影响也很小。因此,QH2的自氧化是一种竞争反应,会降低QH2作为抗氧化剂的有效性,并且不会被SOD或过氧化氢酶减缓。还通过使用在CuZnSOD和/或MnSOD中存在缺失的酵母突变菌株来测试SOD和QH2在体内的相互作用。sod突变酵母菌株每个细胞所含的Q6H2百分比与野生型细胞相同。这些结果表明,QH2的自氧化与SOD无关。

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