氧化磷酸化
线粒体
转位酶
生物
细胞生物学
氧化应激
磷酸化
线粒体内膜
生物化学
染色体易位
基因
作者
Yuek Ling Chai,Huayang Xing,Jenny Chong,Paul T. Francis,Clive Ballard,Christopher Chen,Mitchell K.P. Lai
摘要
Background:The translocase of the outer membrane (TOM) is a vital mitochondrial transport system facilitating the importation of nuclear encoded proteins into the organelle. While mitochondrial dysfunction, including perturbation of oxidative phosphorylation (OXPHOS) complex, is evident in Alzheime r’s disease (AD), it remains unclear whether the observed OXPHOS deficits may be associated with TOM alterations. Objectives:To correlate TOM subunits with OXPHOS complex proteins in AD. Methods:Postmortem neocortex (BA40) from AD and age-matched controls were processed to obtain mitochondrial enriched homogenates for the measurement of Tom20, Tom22, Tom40, and Tom70 as well as components of OXPHOS complex I–V by immunoblotting. Results:Tom20 and Tom70 immunoreactivities were significantly reduced in AD, as were components of OXPHOS complex I and III. Both Tom20 and Tom70 positively correlated with complex III and V, while Tom20 also correlated withcomplex IV. Conclusion:Reductions in certain TOM subunits and their correlations with specific OXPHOS complex proteins suggest that an impaired mitochondrial transportation system may contribute to previously observed oxidative phosphorylation deficits in AD. Follow-up studies are needed to corroborate the present correlative study.
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