Environ Health Toxicol.  2014 ;29(1):e2014001.

New Evidences of Neurotoxicity of Aroclor 1254 in Mice Brain: Potential of Coenzyme Q10 in Abating the Detrimental Outcomes

Affiliations
  • 1Department of Pharmacology, Bombay College of Pharmacy, Kalina, Mumbai, India. amn2720@gmail.com

Abstract


OBJECTIVES
The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain.
METHODS
Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out.
RESULTS
Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard.
CONCLUSIONS
Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.

Keyword

Aroclor 1254; Brain; Coenzyme Q10; Neurotoxicity; Oxidative stress

MeSH Terms

Animals
Aroclors*
Brain*
Catalase
Cats
Chlorodiphenyl (54% Chlorine)*
Cholinesterases
Glutathione
Glutathione Peroxidase
Injections, Intraperitoneal
Lipid Peroxidation
Methods
Mice*
Oxidative Stress
Selegiline
Superoxide Dismutase
Ubiquinone
Aroclors
Catalase
Chlorodiphenyl (54% Chlorine)
Cholinesterases
Glutathione
Glutathione Peroxidase
Selegiline
Superoxide Dismutase
Ubiquinone
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