Methyl-parathion is an OP pesticide that is toxic and can target many organs including the CNS, particularly when metabolized to methyl-paraoxon (the active metabolite). Neurotoxicity is primarily caused by the inhibition of AChE, which results in the accumulation of ACh (Garcia S et al., 2003) and the toxicological cascade described above. Repeated developmental exposure to methyl parathion can induce sex-selective alterations and long-lasting changes in spatial learning and memory formation of rat when measured using a radial arm maze and induce different neurobehavioral outcomes (Johnson FO et al., 2009). Methy-parathion exposure even for short periods of time, may result in alterations in the nervous system and the symptoms arises including headaches, dizziness, confusion, blurred vision, difficulty breathing, vomiting, diarrhea, loss of consciousness, and even death (https://www.atsdr.cdc.gov/ToxProfiles/tp48-c1-b.pdf, 2001). Active metabolite methyl-paraoxon (a AChE inhibitor) is nearly three orders of magnitude more potent than parent compound methyl-parathion (Straus et al., 2000). Methyl-parathion toxicity in both insects and humans is related to the ability of the active oxon metabolite to bind to and inhibit AChE activity (Garcia S et al., 2003).