tailieunhanh - Báo cáo khoa học: Mitochondrial transcription factor A overexpression and base excision repair deficiency in the inner ear of rats with D-galactose-induced aging

Oxidative damage to mtDNA is associated with excessive reactive oxygen species production. The mitochondrial common deletion (mtDNA 4977-bp and 4834-bp deletion in humans and rats, respectively) is the most typical and frequent form of mtDNA damage associated with aging and degenera-tive diseases. | IFEBS Journal Mitochondrial transcription factor A overexpression and base excision repair deficiency in the inner ear of rats with D-galactose-induced aging Yi Zhong1 Yu-Juan Hu1 Bei Chen1 2 Wei Peng1 Yu Sun1 Yang Yang1 Xue-Yan Zhao1 Guo-run Fan1 Xiang Huang3 and Wei-Jia Kong1 1 Department of Otorhinolaryngology Union Hospital Tongji MedicalCollege Huazhong University of Science and Technology Wuhan China 2 Department of Otorhinolaryngology The First Affiliated Hospitalof Zhengzhou University China 3 Institute of Otorhinolaryngology Union Hospital Tongji MedicalCollege Huazhong University of Science and Technology Wuhan China Keywords age-related hearing loss DNA repair mitochondrialcommon deletion mitochondrialtranscription factor A oxidative damage Correspondence W. J. Kong Department of Otorhinolaryngology Union Hospital Tongji Medical College Huazhong University of Science and Technology 1277 Jiefang Avenue Wuhan 430022 China Fax 86 27 85776343 Tel 86 27 85726900 E-mail entwjkong@ These authors contributed equally to this work Received 13 February 2011 revised 21 April 2011 accepted 10 May 2011 doi Oxidative damage to mtDNA is associated with excessive reactive oxygen species production. The mitochondrial common deletion mtDNA 4977-bp and 4834-bp deletion in humans and rats respectively is the most typical and frequent form of mtDNA damage associated with aging and degenerative diseases. The accumulation of the mitochondrial common deletion has been proposed to play a crucial role in age-related 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 D-Gal 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 .