Mitochondrial complex I inhibitor rotenone-induced toxicity and its potential mechanisms in Parkinson's disease models

The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, α-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammati...

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Published inCritical reviews in toxicology Vol. 42; no. 7; pp. 613 - 632
Main Authors Xiong, Nian, Long, Xi, Xiong, Jing, Jia, Min, Chen, Chunnuan, Huang, Jinsha, Ghoorah, Devina, Kong, Xiangquan, Lin, Zhicheng, Wang, Tao
Format Journal Article
LanguageEnglish
Published London Informa Healthcare 01.08.2012
Taylor & Francis
Subjects
alpha-Synuclein - metabolism
Animals
Biological and medical sciences
Corpus Striatum - drug effects
Corpus Striatum - pathology
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Disease Models, Animal
dopaminergic neuron
Dopaminergic Neurons - drug effects
Dopaminergic Neurons - pathology
Humans
Lewy Bodies - drug effects
Lewy Bodies - pathology
mechanism
Medical sciences
Mitochondria - drug effects
Mitochondria - metabolism
Nervous system (semeiology, syndromes)
Nervous system as a whole
neurodegeneration
Neurology
Oxidative Stress - drug effects
Parkinson Disease - etiology
Parkinson Disease - pathology
Parkinson's disease
pathogenesis
Proteolysis - drug effects
rotenone
Rotenone - toxicity
Substantia Nigra - drug effects
Substantia Nigra - pathology
Animal model
Nervous system diseases
Parkinson's disease
Rat
Pathogenesis
Toxicity
Rodentia
Parkinson disease
neurodegeneration
rotenone
Cerebral disorder
Vertebrata
Mitochondria
Mammalia
Mouse
Etiology
Central nervous system disease
Dopaminergic neuron
Degenerative disease
Inhibitor
Mechanism of action
mechanism
Extrapyramidal syndrome
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Abstract The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, α-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammation and loss of neurotrophic factors. Based on a link between mitochondrial dysfunction and pesticide exposure, many laboratories, including ours, have recently developed parkinsonian models by utilization of rotenone, a well-known mitochondrial complex I inhibitor. Rotenone models for PD appear to mimic most clinical features of idiopathic PD and recapitulate the slow and progressive loss of dopaminergic (DA) neurons and the Lewy body formation in the nigral-striatal system. Notably, potential human parkinsonian pathogenetic and pathophysiological mechanisms have been revealed through these models. In this review, we summarized various rotenone-based models for PD and discussed the implied etiology of and treatment for PD
AbstractList The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, α-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammation and loss of neurotrophic factors. Based on a link between mitochondrial dysfunction and pesticide exposure, many laboratories, including ours, have recently developed parkinsonian models by utilization of rotenone, a well-known mitochondrial complex I inhibitor. Rotenone models for PD appear to mimic most clinical features of idiopathic PD and recapitulate the slow and progressive loss of dopaminergic (DA) neurons and the Lewy body formation in the nigral-striatal system. Notably, potential human parkinsonian pathogenetic and pathophysiological mechanisms have been revealed through these models. In this review, we summarized various rotenone-based models for PD and discussed the implied etiology of and treatment for PD
The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, α-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammation and loss of neurotrophic factors. Based on a link between mitochondrial dysfunction and pesticide exposure, many laboratories, including ours, have recently developed parkinsonian models by utilization of rotenone, a well-known mitochondrial complex I inhibitor. Rotenone models for PD appear to mimic most clinical features of idiopathic PD and recapitulate the slow and progressive loss of dopaminergic (DA) neurons and the Lewy body formation in the nigral-striatal system. Notably, potential human parkinsonian pathogenetic and pathophysiological mechanisms have been revealed through these models. In this review, we summarized various rotenone-based models for PD and discussed the implied etiology of and treatment for PD.
Author Kong, Xiangquan
Long, Xi
Xiong, Jing
Lin, Zhicheng
Huang, Jinsha
Xiong, Nian
Chen, Chunnuan
Jia, Min
Wang, Tao
Ghoorah, Devina
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  surname: Xiong
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– sequence: 2
  givenname: Xi
  surname: Long
  fullname: Long, Xi
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  organization: Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 3
  givenname: Jing
  surname: Xiong
  fullname: Xiong, Jing
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 4
  givenname: Min
  surname: Jia
  fullname: Jia, Min
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 5
  givenname: Chunnuan
  surname: Chen
  fullname: Chen, Chunnuan
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 6
  givenname: Jinsha
  surname: Huang
  fullname: Huang, Jinsha
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 7
  givenname: Devina
  surname: Ghoorah
  fullname: Ghoorah, Devina
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 8
  givenname: Xiangquan
  surname: Kong
  fullname: Kong, Xiangquan
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 9
  givenname: Zhicheng
  surname: Lin
  fullname: Lin, Zhicheng
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: 1Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei 430022, China
– sequence: 10
  givenname: Tao
  surname: Wang
  fullname: Wang, Tao
  email: wangtaowh@yahoo.cn, wangtaowh@yahoo.cn
  organization: Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
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Copyright 2012 Informa Healthcare USA, Inc. 2012
2015 INIST-CNRS
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Sun Oct 22 16:09:25 EDT 2023
Tue Jul 04 19:01:42 EDT 2023
Tue Jul 04 19:18:59 EDT 2023
IsPeerReviewed true
IsScholarly true
Issue 7
Keywords Animal model
Nervous system diseases
Parkinson's disease
Rat
Pathogenesis
Toxicity
Rodentia
Parkinson disease
neurodegeneration
rotenone
Cerebral disorder
Vertebrata
Mitochondria
Mammalia
Mouse
Etiology
Central nervous system disease
Dopaminergic neuron
Degenerative disease
Inhibitor
Mechanism of action
mechanism
Extrapyramidal syndrome
Language English
License CC BY 4.0
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Taylor & Francis
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Snippet The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial...
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SubjectTerms alpha-Synuclein - metabolism
Animals
Biological and medical sciences
Corpus Striatum - drug effects
Corpus Striatum - pathology
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Disease Models, Animal
dopaminergic neuron
Dopaminergic Neurons - drug effects
Dopaminergic Neurons - pathology
Humans
Lewy Bodies - drug effects
Lewy Bodies - pathology
mechanism
Medical sciences
Mitochondria - drug effects
Mitochondria - metabolism
Nervous system (semeiology, syndromes)
Nervous system as a whole
neurodegeneration
Neurology
Oxidative Stress - drug effects
Parkinson Disease - etiology
Parkinson Disease - pathology
Parkinson's disease
pathogenesis
Proteolysis - drug effects
rotenone
Rotenone - toxicity
Substantia Nigra - drug effects
Substantia Nigra - pathology
Title Mitochondrial complex I inhibitor rotenone-induced toxicity and its potential mechanisms in Parkinson's disease models
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https://www.ncbi.nlm.nih.gov/pubmed/22574684
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