Paraquat Induces Cell Death Through Impairing Mitochondrial Membrane Permeability

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• 作者：Chuen-Lin Huang ; Chih-Chang Chao ; Yi-Chao Lee ; Mei-Kuang Lu…
• 关键词：Mitochondrial membrane permeability ; Mitochondrial permeability transition pores ; Mitochondrial apoptosis ; induced channels ; Paraquat ; Parkinson’s disease
• 刊名：Molecular Neurobiology
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：53
• 期：4
• 页码：2169-2188
• 全文大小：8,269 KB
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• 作者单位：Chuen-Lin Huang (1) (2)
  Chih-Chang Chao (3)
  Yi-Chao Lee (4)
  Mei-Kuang Lu (5)
  Jing-Jy Cheng (5) (6)
  Ying-Chen Yang (7)
  Vin-Chi Wang (8) (9)
  Wen-Chang Chang (10)
  Nai-Kuei Huang (4) (5) (6)
  
  1. Medical Research Center, Cardinal Tien Hospital, Hsintien, New Taipei City, Taiwan, Republic of China
  2. Graduate Institute of Physiology & Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan, Republic of China
  3. Institute of Neuroscience, National Chengchi University, Taipei, Taiwan, Republic of China
  4. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, 11031, Taiwan, Republic of China
  5. National Research Institute of Chinese Medicine, Ministry of Health and Welfare, 155-1 Li-Nung St., Sec. 2, Shipai, Peitou, Taipei, 112, Taiwan, Republic of China
  6. Institute of Biophotonics, National Yang-Ming University, Taipei, Taiwan, Republic of China
  7. Department of Biotechnology and Animal Science, National Ilan University, Ilan, Taiwan, Republic of China
  8. School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan, Republic of China
  9. Neurological Center, Cardinal Tien Hospital, New Taipei City, Taiwan, Republic of China
  10. Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, 11031, Taiwan, Republic of China
  
• 刊物主题：Neurosciences; Neurobiology; Cell Biology; Neurology;
• 出版者：Springer US
• ISSN：1559-1182

文摘

Paraquat (PQ) as a Parkinsonian mimetic has been demonstrated to impair dopaminergic (DAergic) neurons and is highly correlated with the etiology of Parkinson’s disease (PD) where the death of DAergic neurons has been mainly attributed to impaired mitochondrial functioning. In this study, PQ-induced cytotoxicity focusing on mitochondrial membrane permeability (MMP), which has been implicated to play a part in neurodegeneration, was investigated. Primarily, PQ-induced cytotoxicity and reactive oxygen species (ROS) were inhibited by an inhibitor of NADPH oxidase (NOX), indicating the toxic effect of PQ redox cycling. Further, dibucaine and cyclosporin A which respectively inhibit mitochondrial apoptosis-induced channels (MAC) and mitochondrial permeability transition pores (mPTP) were used and found to prevent PQ-induced mitochondrial dysfunction, such as decreased mitochondrial membrane potential and increased MMP, mitochondrial ROS, and pro-apoptotic factor release. Knockdown of bax and/or bak blocked PQ-induced mitochondrial clusterization of Bax and/or Bak and cytotoxicity, demonstrating the significance of MAC which is composed of Bax and/or Bak. This clusterization coincided with the release of mitochondrial apoptotic factors before there was an increase in inner MMP, indicating that MAC may precede mPTP formation. Besides, NOX inhibitor but not dibucaine attenuated the earlier PQ-induced cytosolic ROS formation or Bax and/or Bak clusterization indicating PQ redox cycling may account for MAC formation. In this model, we have resolved for the first that PQ cytotoxicity through redox cycling may sequentially result in increased outer (MAC) and inner (mPTP) MMP and suggested MMP could be implicated as a therapeutic target in treating neurodegenerative diseases like PD.