Carbofuran, a widely used
carbamate pesticide, has been reported to cause neurotoxicity. However, the underlying mechanisms involved in
carbofuran neurotoxicity are not well understood. The present study was envisaged to investigate the possible role of oxidative stress in
carbofuran neurotoxicity and to evaluate the protective effects of
N-acetylcysteine (NAC).
Acetylcholinesterase activity was significantly inhibited in all the regions of brain after
carbofuran exposure (1 mg/kg
body weight, orally, for 28 days). NAC, on the other hand, was found to partially restore the activity of
acetylcholinesterase in
carbofuran treated animals.
Carbofuran exposure resulted in increased lipid peroxidation (LPO) in brain regions accompanied by decreased levels of
glutathione. NAC administration to the
carbofuran exposed animals lowered LPO along with partial repletion in
glutathione levels. Concomitantly, the activities of
superoxide dismutase,
catalase,
glutathione peroxidase and
glutathione reductase were significantly decreased after
carbofuran exposure, while no significant change in the activity of
glutathione-S-transferase was observed. NAC treatment to
carbofuran treated rats resulted in protective effect on the activities of these
enzymes. Marked impairment in the motor function was seen following
carbofuran exposure, which is evident by significant decrease in the retention time of the rats on rotating rods. Cognitive deficits were also seen after
carbofuran exposure as indicated by the significant decrease in active avoidance response. NAC treatment significantly improved the
carbofuran-induced neurobehavioral deficits. The results clearly demonstrate that
carbofuran exerts its neurotoxic effects by accentuating oxidative stress and suggest neuroprotective role of NAC in
carbofuran neurotoxicity.