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The accumulation of the mitochondrial common deletion has been proposed to play a crucial role in age\u2010related hearing loss (presbycusis). However, the mechanisms underlying the formation and accumulation of mtDNA deletions are still obscure. In the present study, a rat mimetic aging model induced by <jats:sc>d<\/jats:sc>\u2010Gal was used to explore the origin of deletion mutations and how mtDNA repair systems modulate this process in the inner ear during aging. We found that the mitochondrial common deletion was greatly increased and mitochondrial base excision repair capacity was significantly reduced in the inner ear in <jats:sc>d<\/jats:sc>\u2010Gal\u2010treated rats as compared with controls. The overexpression of mitochondrial transcription factor\u2003A induced by <jats:sc>d<\/jats:sc>\u2010Gal significantly stimulated mtDNA replication, resulting in an increase in mtDNA copy number. In addition, an age\u2010related loss of auditory sensory cells in the inner ear was observed in <jats:sc>d<\/jats:sc>\u2010Gal\u2010treated rats. Taken together, our data suggest that mitochondrial base excision repair capacity deficiency and an increase in mtDNA replication resulting from mitochondrial transcription factor\u2003A overexpression may contribute to the accumulation of mtDNA deletions in the inner ear during aging. This study also provides new insights into the development of presbycusis.<\/jats:p>","DOI":"10.1111\/j.1742-4658.2011.08176.x","type":"journal-article","created":{"date-parts":[[2011,5,16]],"date-time":"2011-05-16T15:32:23Z","timestamp":1305559943000},"page":"2500-2510","source":"Crossref","is-referenced-by-count":42,"title":["Mitochondrial transcription factor\u2003A overexpression and base excision repair deficiency in the inner ear of rats with <scp>d<\/scp>\u2010galactose\u2010induced 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