Physiological and Pharmacological study on Buprofezin neurotoxicity and its Reversal by Atropine in Laboratory Rats

Abstract

Buprofezin (BPFN) is a thiadiazine insecticide that inhibits chitin synthesis and the moulting in case of white flies, mealybugs and leaf hoppers. The exposed insects are unable to shed their cuticle and ultimately die as moulting ensue. Neurobehavioral toxic effects elicited by buprofezin remained unclear. Furthermore the reversal of buprofezin induced neurobehavioral toxicity by atropine was not elaborated. Thus, we explored the neurobehavioral toxic consequences of acute buprofezin exposure in adult male rats and effective reversal of these changes by pretreatment with atropine as an antidote. Acute administration of commercial buprofezin (87.9mg/kg/day through oral gavage with com oil as vehicle) induce a wide range of neurobehavioral toxicity including damage to pyramidal cells of hippocampal CAL, CA2 and CA3,region and behavioral irnpainnents as demonstrated through, loss of motor coordination, locomotor activity, fear loss, hearing, heat shock, sensorimotor, cognitive and spatial navigation impairment following the exposure .These neurobehavioral toxic effect of acute buprofezin exposure were significantly reversed by the 15 min pretreatment atropine antidote before the buprofezin administration. Pre-treated atropine (20mg/kg/day;i.p) attenuates the neurobehavioral toxicity induced by buprofezin in adult male rats. Acute buprofezin exposure also induce hematological parameters variation as significant increase in WBCs, lymphocytes, monocytes, red blood cell distribution width and platelets were found following the exposure however pre-treated atropine counteract the effects. It was suggested that acute buprofezin exposure elevated the acetylcholine level, by inhibiting the synthesis and release of acetylcholine esterase (AChE) in synapse. But the complete mechanisms are remained to be elucidated.