Protection of dichlorvos induced oxidative stress and nigrostriatal neuronal death by chronic Coenzyme Q{sub 10} pretreatment

Journal Article · Sat Oct 01 00:00:00 EDT 2011 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/j.taap.2011.07.015· OSTI ID:21587851

Binukumar, BK; Gupta, Nidhi ^[1]; Bal, Amanjit ^[2]

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1. Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012 (India)
2. Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh (India)

Numerous epidemiological studies have shown an association between pesticide exposure and increased risk of developing Parkinson's diseases. Oxidative stress generated as a result of mitochondrial dysfunction has been implicated as an important factor in the etiology of Parkinson's disease. Previously, we reported that chronic dichlorvos exposure causes mitochondrial impairments and nigrostriatal neuronal death in rats. The present study was designed to test whether Coenzyme Q{sub 10} (CoQ{sub 10}) administration has any neuroprotective effect against dichlorvos mediated nigrostriatal neuronal death, {alpha}-synuclein aggregation, and motor dysfunction. Male albino rats were administered dichlorvos by subcutaneous injection at a dose of 2.5 mg/kg body weight over a period of 12 weeks. Results obtained there after showed that dichlorvos exposure leads to enhanced mitochondrial ROS production, {alpha}-synuclein aggregation, decreased dopamine and its metabolite levels resulting in nigrostriatal neurodegeneration. Pretreatment by Coenzyme Q{sub 10} (4.5 mg/kg ip for 12 weeks) to dichlorvos treated animals significantly attenuated the extent of nigrostriatal neuronal damage, in terms of decreased ROS production, increased dopamine and its metabolite levels, and restoration of motor dysfunction when compared to dichlorvos treated animals. Thus, the present study shows that Coenzyme Q{sub 10} administration may attenuate dichlorvos induced nigrostriatal neurodegeneration, {alpha}-synuclein aggregation and motor dysfunction by virtue of its antioxidant action. - Highlights: > CoQ{sub 10} administration attenuates dichlorvos induced nigrostriatal neurodegenaration. > CoQ{sub 10} pre treatment leads to preservation of TH-IR neurons. > CoQ{sub 10} may decrease oxidative damage and {alpha}-synuclin aggregation. > CoQ{sub 10} treatment enhances motor function and protects rats from catalepsy.

• OSTI ID: 21587851
• Journal Information: Toxicology and Applied Pharmacology, Vol. 256, Issue 1; Other Information: DOI: 10.1016/j.taap.2011.07.015; PII: S0041-008X(11)00284-5; Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
AGGLOMERATION
COENZYMES
DOPAMINE
ETIOLOGY
HYDROXYLASES
MALES
MITOCHONDRIA
NERVE CELLS
NERVOUS SYSTEM DISEASES
OXIDATION
OXYGEN
SAFETY
STRESSES
SUBCUTANEOUS INJECTION
TYROSINE
AMINES
AMINO ACIDS
ANIMAL CELLS
AROMATICS
AUTONOMIC NERVOUS SYSTEM AGENTS
CARBOXYLIC ACIDS
CARDIOTONICS
CARDIOVASCULAR AGENTS
CELL CONSTITUENTS
CHEMICAL REACTIONS
DISEASES
DRUGS
ELEMENTS
ENZYMES
HYDROXY ACIDS
HYDROXY COMPOUNDS
INJECTION
INTAKE
NEUROREGULATORS
NONMETALS
ORGANIC ACIDS
ORGANIC COMPOUNDS
OXIDOREDUCTASES
PHENOLS
POLYPHENOLS
PROTEINS
SOMATIC CELLS
SYMPATHOMIMETICS