Jornal de Toxicologia Clínica
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Atropine Reverts the Neurobehavioral Toxicity Elicited by Acute Exposure to Buprofezin in Sprague Dowley Rats

Muhammad Aslam

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 (87.9 mg/kg/day through oral gavage with corn oil as vehicle) induce a wide range of neurobehavioral toxicity including damage to pyramidal cells of hippocampal Carnu Ammonis (CA1), and CA3, region and behavioral impairments 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 pre- treatment of atropine antidote before the buprofezin administration. Pre-treated atropine (20 mg/kg/day; IP) attenuates the neurobehavioral toxicity induced by buprofezin in adult male rats. 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.