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首页> 外文期刊>American Journal of Physiology >Oxidized low-density lipoprotein and 15-deoxy-delta 12,14-PGJ2 increase mitochondrial complex I activity in endothelial cells.
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Oxidized low-density lipoprotein and 15-deoxy-delta 12,14-PGJ2 increase mitochondrial complex I activity in endothelial cells.

机译：氧化的低密度脂蛋白和15-脱氧-δ12,14-PGJ2增加了内皮细胞中线粒体复合物I的活性。

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摘要

Oxidized lipids are capable of initiating diverse cellular responses through both receptor-mediated mechanisms and direct posttranslational modification of proteins. Typically, exposure of cells to low concentrations of oxidized lipids induces cytoprotective pathways, whereas high concentrations result in apoptosis. Interestingly, mitochondria can contribute to processes that result in either cytoprotection or cell death. The role of antioxidant defenses such as glutathione in adaptation to stress has been established, but the potential interaction with mitochondrial function is unknown and is examined in this article. Human umbilical vein endothelial cells (HUVEC) were exposed to oxidized LDL (oxLDL) or the electrophilic cyclopentenone 15-deoxy-Delta 12,14-PGJ2 (15d-PGJ2). We demonstrate that complex I activity, but not citrate synthase or cytochrome-c oxidase, is significantly induced by oxLDL and 15d-PGJ2. The mechanism is not clear at present but is independent of the induction of GSH, peroxisome proliferator-activated receptor (PPAR)-gamma, and PPAR-alpha. This response is dependent on the induction of oxidative stress in the cells because it can be prevented by nitric oxide, probucol, and the SOD mimetic manganese(III) tetrakis(4-benzoic acid) porphyrin chloride. This increased complex I activity appears to contribute to protection against apoptosis induced by 4-hydroxynonenal.
机译：氧化的脂质能够通过受体介导的机制和蛋白质的直接翻译后修饰来引发多种细胞应答。通常，将细胞暴露于低浓度的氧化脂质会诱导细胞保护途径，而高浓度会导致细胞凋亡。有趣的是，线粒体可以促进导致细胞保护或细胞死亡的过程。谷胱甘肽等抗氧化剂防御在适应压力中的作用已经确立，但与线粒体功能的潜在相互作用尚不清楚，本文对此进行了研究。将人脐静脉内皮细胞（HUVEC）暴露于氧化的LDL（oxLDL）或亲电的环戊烯酮15-脱氧-δ12,14-PGJ2（15d-PGJ2）。我们证明，oxLDL和15d-PGJ2可显着诱导复杂的I活性，而不是柠檬酸合酶或细胞色素C氧化酶。该机制目前尚不清楚，但与GSH，过氧化物酶体增殖物激活受体（PPAR）-γ和PPAR-α的诱导无关。该反应取决于细胞中氧化应激的诱导，因为它可以被一氧化氮，普罗布考和SOD模拟锰（III）四（4-苯甲酸）卟啉氯化物所阻止。这种增加的复合物I活性似乎有助于抵抗4-羟基壬烯醛诱导的细胞凋亡。

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