Studies on the Effect of Fipronil Insecticide on Some Brain Regions of Male Albino Rats

Abstract

Fipronil (FIP) is a widely used insecticide for many purposes in different application fields including Veterinary Medicine, agriculture and public health. The extensive usage of FIP may lead to environmental pollution and non-intentional exposure of non-target species. FIP was reported to have a neurotoxic effect against insects, and it also showed neurological hazard upon vertebrate exposure. However, slight is known about its potential neurotoxic effects and its molecular mechanisms on the non-target organisms. Therefore, this study aimed to assess apoptosis, oxidative stress, genotoxicity, neuroinflammation and histopathological alterations in discrete brain regions; cerebral cortex , hippocampus, caudate and putamen, cerebellum, brain stem and diencephalon after sub-acute exposure of rats to FIP. Twenty adult male albino rats were divided into 2 groups (10 rats/ group), control group and FIP treated group. Each rat of the treated group received a daily dose of FIP (technical grade) at 10 mg/kg body weight by oral gavage for 45 days. The discrete brain regions were processed to examine oxidative stress induced macromolecular modifications. Besides, Tumor necrosis factor-α (TNF- α )and B - cell lymphoma 2 (Bcl-2) gene expression and immunoreactivity for caspase-3 (active form), inducible nitric oxide synthase(iNOS) and glial fibrillary acidic protein (GFAP) were evaluated. In addition, histopathological assessment was performed. Our results revealed that FIP significantly raised malondialdehyde (MDA), protein carbonyls and DNA fragmentation (p≤0.05). Also, significant increased immunoreactivity of GFAP, iNOS, caspase-3 (active form) in FIP treated group was noticed (p≤0.05). Histopathologically, histoarchitectural distortion and neuronal degeneration in these regions were observed. In conclusion, the current study suggests the ability of FIP to induce oxidative stress mediated macromolecular alterations, leading to apoptosis and tissue reaction in these brain regions, with variable susceptibility of these regions to the induced oxidative stress and the subordinated events