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Free Radic Biol Med. 2013 Oct;63:30-40. doi: 10.1016/j.freeradbiomed.2013.04.030. Epub 2013 Apr 30.

Comparative bioenergetic study of neuronal and muscle mitochondria during aging.

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1
School of Life Science, Wenzhou Medical College, Wenzhou, Zhejiang 325035, China.

Erratum in

  • Free Radic Biol Med. 2016 Feb;91:203.

Abstract

Mitochondrial respiratory chain defects have been associated with various diseases and with normal aging, particularly in tissues with high energy demands, including brain and skeletal muscle. Tissue-specific manifestation of mitochondrial DNA (mtDNA) mutations and mitochondrial dysfunction are hallmarks of mitochondrial diseases although the underlying mechanisms are largely unclear. Previously, we and others have established approaches for transferring mtDNA from muscle and synaptosomes of mice at various ages to cell cultures. In this study, we carried out a comprehensive bioenergetic analysis of cells bearing mitochondria derived from young, middle-aged, and old mouse skeletal muscles and synaptosomes. Significant age-associated alterations in oxidative phosphorylation and regulation during aging were observed in cybrids carrying mitochondria from both skeletal muscle and synaptosomes. Our results also revealed that loss of oxidative phosphorylation capacity may occur at various ages in muscle and brain. These findings indicate the existence of a tissue-specific regulatory mechanism for oxidative phosphorylation.

KEYWORDS:

Aging; Cybrid; Free radicals; Mitochondria; Skeletal muscle; Synaptosome

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