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Publication : Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging.

First Author  Kujoth GC Year  2005
Journal  Science Volume  309
Issue  5733 Pages  481-4
PubMed ID  16020738 Mgi Jnum  J:99764
Mgi Id  MGI:3583732 Doi  10.1126/science.1112125
Citation  Kujoth GC, et al. (2005) Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging. Science 309(5733):481-4
abstractText  Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.
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