Involvement of acetylcholinesterase inhibition in paralyzing effects of monocrotophos in Caenorhabditis elegans

Abstract

Organophosphorus insecticides (OPI) are among the most commonly used class of pesticides in agricultural and domestic scenarios. Clinical presentations of acute OPI toxicity are attributable to acetylcholinesterase inhibition and ensuing cholinergic stress. Consequently, acetylcholinesterase reactivators and acetylcholine receptor antagonists are used to treat clinical cases of OPI toxicity. The nematode worm Caenorhabditis elegans is emerging as an attractive alternative model for toxicity evaluations. This study was carried out to understand the involvement of acetylcholinesterase inhibition in paralyzing effects of monocrotophos (an OPI) in Caenorhabditis elegans. Exposure of C. elegans to monocrotophos was associated with strong toxicity in an acute toxicity test as revealed by LC50 of 35.5 ± 1.2 mM. Sub-lethal concentrations of monocrotophos were found to elicit severe acetylcholinesterase inhibition and paralysis. Co-exposure of worms to pralidoxime was found to rescue worms from the paralyzing effects of monocrotophos along with partial reactivation of acetylcholinesterase activity. Our work demonstrates that acetylcholinesterase inhibition is responsible for the paralyzing effects of monocrotophos in Caenorhabditis elegans, and paralysis can be used as an experimental marker of cholinergic acute toxicity of OPI in C. elegans.