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

Critical Reviews in Toxicology
N XiongT Wang

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.

References

Feb 1, 1989·Journal of Neurochemistry·P RiedererM B Youdim
Mar 4, 2000·Toxicological Sciences : an Official Journal of the Society of Toxicology·J S Isenberg, J E Klaunig
Sep 16, 2000·Biochemical Society Symposium·J T GreenamyreS E Stephans
Dec 2, 2000·Nature Neuroscience·R BetarbetJ T Greenamyre
Jul 5, 2001·Environmental Research·A PriyadarshiS S Priyadarshi
Apr 12, 2002·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·Ranjita BetarbetJ Timothy Greenamyre
May 2, 2002·The Journal of Neuropsychiatry and Clinical Neurosciences·James Parkinson
Sep 17, 2002·Molecular Therapy : the Journal of the American Society of Gene Therapy·Byoung Boo SeoAkemi Matsuno-Yagi
Oct 3, 2002·Journal of Neurochemistry·Anatoly A StarkovGary Fiskum
Nov 20, 2002·Journal of Neurochemistry·Xiaoxia WangM Catherine Bennett
Dec 25, 2002·Neurobiology of Aging·Heiko BraakEva Braak
Feb 1, 2003·Journal of Neurochemistry·Günter U HöglingerEtienne C Hirsch
Jul 9, 2003·Annals of the New York Academy of Sciences·Gary FiskumChristos Chinopoulos
Oct 8, 2003·Current Medicinal Chemistry·Y Kotake, S Ohta
Nov 19, 2003·Journal of Neurochemistry·Ferogh A AhmadiW Michael Zawada
Feb 10, 2004·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Nicolas LapointeFrancesca Cicchetti
Feb 21, 2004·Toxicological Sciences : an Official Journal of the Society of Toxicology·Kathleen NewhouseZhengui Xia
Jun 17, 2004·Human Molecular Genetics·Houbo JiangJian Feng
Jul 22, 2004·Behavioural Brain Research·M Alam, W J Schmidt
Jul 29, 2004·The Journal of Pharmacology and Experimental Therapeutics·Masahiko Watabe, Toshio Nakaki
Sep 29, 2004·Neurotoxicology and Teratology·Sandrine BretaudSu Guo
Oct 27, 2004·Cell and Tissue Research·Andreas Schober
Dec 3, 2004·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Hélène Coulom, Serge Birman
Mar 26, 2005·Brain Research. Molecular Brain Research·Claudia M TestaJ Timothy Greenamyre
Apr 28, 2005·Brain Research·Fabio García-GarcíaJames M Krueger
May 14, 2005·Antioxidants & Redox Signaling·April A DukesTeresa G Hastings
May 14, 2005·Antioxidants & Redox Signaling·Serge Przedborski, Harry Ischiropoulos

❮ Previous
Next ❯

Citations

Oct 10, 2013·The International Journal of Biochemistry & Cell Biology·Quan HeXianlin Han
Mar 19, 2013·Behavioral and Brain Functions : BBF·Nian XiongTao Wang
Sep 3, 2013·Assay and Drug Development Technologies·Christophe AntczakHakim Djaballah
May 23, 2014·Translational Neurodegeneration·Shweta ModgilAkshay Anand
Jan 13, 2015·Molecular Neurobiology·Jing XiongTao Wang
May 20, 2015·The Veterinary Journal·K SaekiT Nakagawa
Oct 12, 2014·Toxicological Sciences : an Official Journal of the Society of Toxicology·Qian ZhouLong Chen
May 4, 2016·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Nian XiongZhicheng Lin
Jun 28, 2016·Antioxidants & Redox Signaling·Franziska SotznyElke Krüger
Mar 14, 2017·Toxicology Letters·Terry R Van VleetEric A G Blomme
Aug 29, 2013·Arquivos de neuro-psiquiatria·Marcela Augusta de Souza PinhelDorotéia Rossi Silva Souza
Dec 18, 2014·Annals of the New York Academy of Sciences·Jorge S ValadasPatrik Verstreken
May 24, 2017·Toxicology Mechanisms and Methods·Xiao-Wen JiangWen-Hui Yu
May 11, 2019·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Wen Yuan LuoHong Zhang
Apr 8, 2015·Drug Development Research·Kodeeswaran ParameshwaranCarl A Pinkert
Jan 18, 2018·Critical Reviews in Analytical Chemistry·Anantharaman Shivakumar, M S Yogendra Kumar
Sep 15, 2019·Journal of Molecular Neuroscience : MN·Zuhair I AbdullaMatthew R Skelton
Jan 10, 2020·Neuromolecular Medicine·Debapriya Garabadu, Nidhi Agrawal
Nov 28, 2019·The International Journal of Neuroscience·İsmail ÜnalEbru Emekli-Alturfan
Sep 6, 2019·Apoptosis : an International Journal on Programmed Cell Death·Mengqiu WuZhanjun Jia
Feb 16, 2017·Frontiers in Molecular Neuroscience·Jinsha HuangTao Wang
Jun 21, 2013·Molecular Medicine Reports·Yu WangQunying Fu
Jun 6, 2018·Frontiers in Physiology·Sandra M Cardoso, Nuno Empadinhas

❮ Previous
Next ❯

Related Concepts

Related Feeds

Basal Ganglia

Basal Ganglia are a group of subcortical nuclei in the brain associated with control of voluntary motor movements, procedural and habit learning, emotion, and cognition. Here is the latest research.

Alpha-Synuclein Aggregation

Alpha-synucleins are small proteins that are believed to restrict the mobility of synpatic vesicles and inhibit neurotransmitter release. Aggregation of these proteins have been linked to several types of neurodegenerative diseases including dementia with Lewy bodies and Parkinson's disease. Here is the latest research on α-synuclein aggregation.

Alpha-Synuclein Aggregation (MDS)

Alpha-synucleins are small proteins that are believed to restrict the mobility of synpatic vesicles and inhibit neurotransmitter release. Aggregation of these proteins have been linked to several types of neurodegenerative diseases including dementia with Lewy bodies and Parkinson's disease. Here is the latest research on α-synuclein aggregation.