Abstract
Abstract Background: The organophosphorus compound dimethoate is pesticide that widely used across the world to control worms and insects. It is highly toxic and causes neurobehavioral disorders. Quercetin is a natural flavonoid that is profusely found in fruits and vegetablesand is known for its antioxidants property and its ability to improve oxidative stress and promote cellular survival. Aim of Study: To assess neurotoxicity and structural alterations of cerebellar cortex caused by dimethoate and explore the neuroprotective potential effect of quercetin. Material and Methods: The study was carried out on 32 adult, male Wister albino rats weighing 180-200g, they were randomly divided into four groups: Normal control, dimethoate treated (30mg/kg alternate day), quercetin treated (50mg/kg daily) and combined dimethoate + quercetin treated. All the treatments continued for 60 days. All animals were anesthe-tized, cerebellum was removed to prepare the specimens for histological, immunohistochemical and biochemical exami-nation. Results: The results revealed asign of toxicity and a significant decrease in body weight of animals treated with dimethoate which were substantially improved upon concurrent supplementation with quercetin. Further, treatment with dimethoate resulted in a significant decrease in the activity of acetyl cholinesterase in cerebellum tissue which was increased upon co-treatment with quercetin. On the contrary, we noticed a significant increase in the levels of MDA in cerebellum which were revealed significant reduction upon supplementation of quercetin. Light microscopic examination of cerebellum showed histoarchitectural alterations with significant up regulation of apoptotic marker (caspase-3) and astrogliosis marker Glial Fibrillary Acidic Protein (GFAP) in cerebellar tissue, Although, there were a significant down regulation of synaptophysin (SYP) immunoexpression. These changes were improved upon co-treatment with quercetin. Therefore, we conclude that quercetin when used as a prophy-lactic intervention would afford safeguard against dimethoate induced neurotoxicity.
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