Alterations in the Acetylcholinesterase Activity in the Brain of Albino Mice Exposed to Acephate

Acephate (AP), an organophosphorus (OP) insecticide, is considered as one of the safest OP insecticides because of its low mammalian toxicity. AP is rapidly and extensively metabolized to a more potent OP insecticide methamidophos (MP), which has a lower LD50 in mice and rats, thus a higher toxicity than AP (Spassova et al., 2000; Tanaka et al., 2005). Earlier reports issued by the Food and Agriculture Organization of the United Nations have indicated that urinary levels of MP and other metabolites are measureable in human subjects exposed to AP in formulation plants. Reports of acute human exposures to AP are extremely limited. Other reports indicate that chronic exposure in workers in industrial AP manufacturing has resulted in measurable urinary levels of AP, but not MP and no depression of AChE activity (Maroni et al., 1990). AP exposure in humans results in bradycardia/ tachycardia, central nervous system impairment, eye problems, gastrointestinal problems and respiratory problems and finally death due to respiratory failure. AP toxicity studies were done mostly in rats. Nakuleswar Dut et al (2013) studied the effect of acephate on accessory sex organs in male rats. The toxic effects of AP are not extensively studied in mice. In this paper we report the toxic effect of acephate on cholinergic mechanisms in different regions of the brain in mice exposed to sub-lethal AP toxicity.