The role of peroxiredoxin III in the ototoxic drug-induced mitochondrial apoptosis of cochlear hair cells
Conclusion. Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells. Objectives. The aim of the present study was to investigate the effects of the depletion of endogenous Prx III on oxidative damage t...
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Published in | Acta oto-laryngologica Vol. 128; no. 9; pp. 944 - 951 |
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Main Authors | , , , , , |
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Language | English |
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Informa UK Ltd
01.01.2008
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Abstract | Conclusion. Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells. Objectives. The aim of the present study was to investigate the effects of the depletion of endogenous Prx III on oxidative damage to mitochondrial components and on apoptotic events with the use of RNA interference. Materials and methods. Depletion of Prx III was done by RNA interference in cochlear hair cells (UB/OC-1), and cells were exposed to ototoxic drugs (cisplatin or gentamicin). We then compared the apoptotic signaling between Prx III-depleted and control cells. Results. The depletion of Prx III resulted in increased intracellular ROS levels accompanied by enhanced apoptosis by ototoxic drugs. The Prx III-depleted cells showed mitochondrial membrane potential collapse, cytochrome c release, and caspase activation. |
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AbstractList | CONCLUSIONPeroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells.OBJECTIVESThe aim of the present study was to investigate the effects of the depletion of endogenous Prx III on oxidative damage to mitochondrial components and on apoptotic events with the use of RNA interference.MATERIALS AND METHOD. Depletion of Prx III was done by RNA interference in cochlear hair cells (UB/OC-1), and cells were exposed to ototoxic drugs (cisplatin or gentamicin). We then compared the apoptotic signaling between Prx III-depleted and control cells.RESULTSThe depletion of Prx III resulted in increased intracellular ROS levels accompanied by enhanced apoptosis by ototoxic drugs. The Prx III-depleted cells showed mitochondrial membrane potential collapse, cytochrome c release, and caspase activation. Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells. The aim of the present study was to investigate the effects of the depletion of endogenous Prx III on oxidative damage to mitochondrial components and on apoptotic events with the use of RNA interference. . Depletion of Prx III was done by RNA interference in cochlear hair cells (UB/OC-1), and cells were exposed to ototoxic drugs (cisplatin or gentamicin). We then compared the apoptotic signaling between Prx III-depleted and control cells. The depletion of Prx III resulted in increased intracellular ROS levels accompanied by enhanced apoptosis by ototoxic drugs. The Prx III-depleted cells showed mitochondrial membrane potential collapse, cytochrome c release, and caspase activation. Conclusion. Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells. Objectives. The aim of the present study was to investigate the effects of the depletion of endogenous Prx III on oxidative damage to mitochondrial components and on apoptotic events with the use of RNA interference. Materials and methods. Depletion of Prx III was done by RNA interference in cochlear hair cells (UB/OC-1), and cells were exposed to ototoxic drugs (cisplatin or gentamicin). We then compared the apoptotic signaling between Prx III-depleted and control cells. Results. The depletion of Prx III resulted in increased intracellular ROS levels accompanied by enhanced apoptosis by ototoxic drugs. The Prx III-depleted cells showed mitochondrial membrane potential collapse, cytochrome c release, and caspase activation. |
Author | Yi Park, Hun Chul Hwang, Sung Sun Kim, Young Seok Choi, Ho Park, Keehyun Joo Park, Kwang |
Author_xml | – sequence: 1 givenname: Ho surname: Seok Choi fullname: Seok Choi, Ho email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon – sequence: 2 givenname: Kwang surname: Joo Park fullname: Joo Park, Kwang email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon – sequence: 3 givenname: Sung surname: Chul Hwang fullname: Chul Hwang, Sung email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon – sequence: 4 givenname: Hun surname: Yi Park fullname: Yi Park, Hun email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon – sequence: 5 givenname: Young surname: Sun Kim fullname: Sun Kim, Young email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon – sequence: 6 givenname: Keehyun surname: Park fullname: Park, Keehyun email: parkkh@ajou.ac.kr organization: 1Department of Otorhinolaryngology-Head & Neck Surgery, Inha University College of Medicine, Incheon |
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Keywords | Antineoplastic agent Drug Hair cell of the ear Toxicity Gentamicin ENT Antioxidant Cisplatin Alkylating agent Antibiotic Mitochondria Aminoglycoside ROS Cochlea Protein synthesis inhibitor Antibacterial agent Platinum II Complexes Apoptosis Ototoxicity |
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Snippet | Conclusion. Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear... Peroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair cells. The... CONCLUSIONPeroxiredoxin (Prx) III plays a protective role in cisplatin- and gentamicin-induced apoptosis via a mitochondria-dependent pathway in cochlear hair... |
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SubjectTerms | Anti-Bacterial Agents - pharmacology Antineoplastic Agents - pharmacology antioxidant Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences Cell Culture Techniques cisplatin Cisplatin - pharmacology Cochlea - drug effects Cochlea - metabolism Cochlea - pathology gentamicin Gentamicins - pharmacology Hair Cells, Auditory - drug effects Hair Cells, Auditory - metabolism Hair Cells, Auditory - pathology Humans In Situ Nick-End Labeling Medical sciences Mitochondria - drug effects Mitochondria - metabolism Mitochondria - pathology Otorhinolaryngology. Stomatology ototoxicity Oxidative Stress - drug effects Oxidative Stress - physiology Peroxiredoxin III Peroxiredoxins - physiology Reactive Oxygen Species - metabolism RNA Interference ROS |
Title | The role of peroxiredoxin III in the ototoxic drug-induced mitochondrial apoptosis of cochlear hair cells |
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