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      Mitochondrial complex I inhibition as a possible mechanism of chlorpyrifos induced neurotoxicity

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          Abstract

          Background

          Organophosphates (OPs) represent the most widely used class of pesticides. Although perceived as low toxicity compounds compared to the previous organochlorines, they still possess neurotoxic effects both on acute and delayed levels. Delayed neurotoxic effects of OPs include OPIDN and OPICN. The mechanisms of these delayed effects have not been totally unraveled yet. One possible contributor for neurotoxicity is mitochondrial complex I (CI) inhibition.

          Purpose

          in the present study we evaluated the contributing role of (CI) inhibition in chlorpyrifos (CPF) induced delayed neuropathy in hens.

          Methods

          Experimented birds received 150 mg/kg of CPF, and evaluated behaviorally and biochemically.

          Results

          CPF treated hens received 150 mg/kg and developed signs of delayed neurotoxicity, which were verified by NTE inhibition. These effects were paralleled by CI inhibition and decrease in ATP level.

          Conclusions

          The data confirms the possible role of CI inhibition in CPF induced delayed neuropathy.

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          Most cited references26

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          A simplified method of evaluating dose-effect experiments.

          J LITCHFIELD, F WILCOXON (1949)
          Article 0 comments Cited 232 times – based on 0 reviews     Review now
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            Health effects of chronic pesticide exposure: cancer and neurotoxicity.

            Jane Hoppin, Michael Alavanja, Freya Kamel (2003)
            Pesticides are widely used in agricultural and other settings, resulting in continuing human exposure. Epidemiologic studies indicate that, despite premarket animal testing, current exposures are associated with risks to human health. In this review, we describe the routes of pesticide exposures occurring today, and summarize and evaluate the epidemiologic studies of pesticide-related carcinogenicity and neurotoxicity in adults. Better understanding of the patterns of exposure, the underlying variability within the human population, and the links between the animal toxicology data and human health effects will improve the evaluation of the risks to human health posed by pesticides. Improving epidemiology studies and integrating this information with toxicology data will allow the human health risks of pesticide exposure to be more accurately judged by public health policy makers.
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              The mitochondrial complex I inhibitor rotenone triggers a cerebral tauopathy.

              W. Oertel, Andrew P. Michel, Myriam Khondiker … (2005)
              Reduced activity of the mitochondrial respiratory chain--particularly complex I--may be implicated in the etiology of both Parkinson's disease and progressive supranuclear palsy, although these neurodegenerative diseases differ substantially as to their distinctive pattern of neuronal cell loss and the predominance of cerebral alpha-synuclein or tau protein pathology. To determine experimentally whether chronic generalized complex I inhibition has an effect on the distribution of alpha-synuclein or tau, we infused rats systemically with the plant-derived isoflavonoid rotenone. Rotenone-treated rats with a pronounced metabolic impairment had reduced locomotor activity, dystonic limb posture and postural instability. They lost neurons in the substantia nigra and in the striatum. Spherical deposits of alpha-synuclein were observed in a few cells, but cells with abnormal cytoplasmic accumulations of tau immunoreactivity were significantly more numerous in the striatum of severely lesioned rats. Abnormally high levels of tau immunoreactivity were found in the cytoplasm of neurons, oligodendrocytes and astrocytes. Ultrastructurally, tau-immunoreactive material consisted of straight 15-nm filaments decorated by antibodies against phosphorylated tau. Many tau+ cell bodies also stained positive for thioflavin S, nitrotyrosine and ubiquitin. Some cells with abnormal tau immunoreactivity contained activated caspase 3. Our data suggest that chronic respiratory chain dysfunction might trigger a form of neurodegeneration in which accumulation of hyperphosphorylated tau protein predominates over deposits of alpha-synuclein.
              Article 0 comments Cited 60 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Neurosci
                Journal ID (iso-abbrev): Ann Neurosci
                Journal ID (publisher-id): ANS
                Title: Annals of Neurosciences
                Publisher: Indian Academy of Neurosciences
                ISSN (Print): 0972-7531
                ISSN (Electronic): 0976-3260
                Publication date (Print): July 2014
                Volume: 21
                Issue: 3
                Pages: 85-89
                Affiliations
                [1 ]Toxicology Department;
                [2 ]Medical Experimental Research Center (MERC)-Mansoura University;
                [3 ]Clinical pharmacology department, Menoufia Medical School, Menoufia University, Egypt
                Author notes
                [* ]Corresponding Author: +201-20268881 wmy107@ 123456gmail.com
                Article
                Publisher ID: 210303
                DOI: 10.5214/ans.0972.7531.210303
                PMC ID: 4158778
                PubMed ID: 25206071
                SO-VID: 3ea10205-f428-474d-bdf7-bb3b4db84aea
                Copyright © Copyright © 2014, The National Academy of Sciences
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 25 April 2014
                Date revision received : 23 May 2014
                Date accepted : 7 July 2014
                Categories
                Subject: Research Article
                Subject: Clinical Neuroscience

                Keywords: ops,cpf,ci,opidn,esterases,mitochondria
                Data availability:
                Keywords: ops, cpf, ci, opidn, esterases, mitochondria

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