The Role of Peroxiredixin Ⅲ in the ototoxic drug-induced mitochondrial apoptosis of cochlear hair cell

Apoptosis is essential during development and for maintenance of healthy tissues. Dysregulation of apoptosis has thus been found to contribute to many pathologies, including neurodegenerative disorders, as well as to tumor promotion. Normal cellular processes that involves oxygen result in the production of reactive oxygen species. Intracellular H2O2 is removed mostly by catalase, glutathione peroxidase, and peroxiredoxin(Prx). The newly identified Prx family of peroxidases includes at least six isoforms in mammalian cells. Among them, Prx III is synthesized with a mitochondrial targeting sequence and is then transferred to mitochondria. We have shown that Prx III is an important, if not the most important, H2O2-eliminating enzyme in mitochondria and that the mitochondrial generation of H2O2 contributes to apoptotic signaling independently of the direct contribution of O2-. The intracellular accumulation of H2O2 caused by Prx III depletion resulted in accumulation of apoptosis, with increased rates of mitochondrial membrane potential collapse, cytochrome c relaease, and caspase activation. In conclusion, we demonstrated that cisplatin, gentamycin induced apoptosis was related to mitochondria-dependant pathyway through interaction with H2O2 and Prx III.

Author dc:creator

• 최, 호석

Contributors dc:contributor

• 박, 기현
• 대학원 의학과
• 103280

• Peroxiredoxin
• siRNA
• ototoxic
• drug
• apoptosis

Language dc:language

ko

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000001863
000000001863

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/1618