Dicarbonyls linked to damage in the powerhouse: glycation of mitochondrial proteins and oxidative stress.
Dicarbonyls linked to damage in the powerhouse: glycation of mitochondrial proteins and oxidative stress.
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DOI：
10.1042/bst0361045
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发表时间：
2008-10
影响因子：
3.9
通讯作者：
Thornalley, Paul J.
中科院分区：
文献类型：
--
作者：
Rabbani, Naila;Thornalley, Paul J.
保护线粒体蛋白免受内源性二羰基化合物，甲基乙二醛和乙二醛，最近发现，以防止增加的活性氧的形成和氧化和亚硝化损伤的蛋白质组在老化过程中，并产生寿命延长线虫线虫。这表明线粒体蛋白质组的二羰基糖化损伤可能是导致氧化应激的线粒体功能障碍的前一事件。未来的研究将解决线粒体蛋白中的功能电荷，这是二羰基糖化的目标。
Protection of mitochondrial proteins from glycation by endogenous dicarbonyl compounds, methylglyoxal and glyoxal, was found recently to prevent increased formation of reactive oxygen species and oxidative and nitrosative damage to the proteome during aging and produce life extension in the nematode Caenorhabditis elegans. This suggests that dicarbonyl glycation damage to the mitochondrial proteome may be a preceding event to mitochondrial dysfunction leading to oxidative stress. Future research will address the functional charges in mitochondrial proteins that are the targets for dicarbonyl glycation.