Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

Abstract

Organophosphorus insecticides including chlorpyrifos (CPF) are mainly used for agriculture, household, and military purposes; their application is associated with various adverse reactions in animals and humans. This study was conducted to evaluate the potential neuroprotective effect of red beetroot methanolic extract (RBR) against CPF-induced cortical damage. Twenty-eight adult male Wistar albino rats were divided into 4 groups (n=7 in each group): the control group was administered physiological saline (0.9% NaCl), the CPF group was administered CPF (10 mg/kg), the RBR group was administered RBR (300 mg/kg), and the RBR+CPF group was treated with RBR (300 mg/kg) 1 hr before CPF (10 mg/kg) supplementation. All groups were treated for 28 days. Rats exposed to CPF exhibited a significant decrease in cortical acetylcholinesterase activity and brain-derived neurotrophic factor and a decrease in glial fibrillary acidic protein. CPF intoxication increased lipid peroxidation, inducible nitric oxide synthase expression, and nitric oxide production. This was accompanied by a decrease in glutathione content and in the activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase in the cortical tissue. Additionally, CPF enhanced inflammatory response, indicated by increased levels and expression of interleukin-1β and tumor necrosis factor-α. CPF triggered neuronal apoptosis by upregulating Bax and caspase-3 and downregulating Bcl-2. However, RBR reversed the induced neuronal alterations following CPF intoxication. Our findings suggest that RBR can minimize and prevent CPF neurotoxicity through its antioxidant, anti-inflammatory, and antiapoptotic activities.

Antioxidant and Anti-Inflammatory Potential of Thymoquinone and Lycopene Mitigate the Chlorpyrifos-Induced Toxic Neuropathy

“…These findings are congruent with those obtained by preceding research by AlKahtane et al [ 7 ], Fereidouni et al [ 37 ], and Mahmoud et al [ 10 ], who demonstrated that CPF induces neurotoxicity associated with lowered levels of AchE. Similarly, decreased serum levels of AchE may be a reverberation of its diminished activity in the brain after CPF-stimulated cholinergic transmission disruption [ 5 ].…”

“…In addition to AchE suppression, other evidence proposed that excessive production of ROS and lipid peroxidation (LPO) are other mechanisms implicated in CPF-induced neuropathy [ 5 , 9 , 10 ]. ROS (hydroxyl radical, OH • ; hydrogen peroxide, H 2 O 2 ; superoxide anion, O 2 •− ) and reactive nitrogen species (nitric oxide, NO and peroxynitrite, ONOO − ) are reported to be invigorated during CPF intoxication as a result of exhaustion of the endogenous antioxidant molecules [ 5 , 7 , 35 ]. Verma et al [ 6 ] has documented alterations in the antioxidant system, including superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) in CPF-intoxicated rats.…”

“…Our oxidative/antioxidants appeared consistent with those obtained by previous reports that revealed incompetency in the cellular antioxidants in the neuronal tissue following CPF exposure [ 9 , 10 ]. Besides, Albasher et al [ 5 ] has used the CPF as a model for induction of oxidative hurt in the brain tissue. Because of the higher lipid content of the brain, lower antioxidant levels, and rapid oxygen exhaustion, the brain was more vulnerable to the progression of oxidative stress compared to other body organs.…”

“…In addition to AchE suppression, other evidence proposed that excessive production of ROS and lipid peroxidation (LPO) are other mechanisms implicated in CPF-induced neuropathy [5,9,10]. ROS (hydroxyl radical, OH • ; hydrogen peroxide, H 2 O 2 ; superoxide anion, O 2…”

“…The indiscriminate utilization of CPF has procured in mounting disquiet about their potential toxic impacts [ 4 ]. CPF and its metabolite chlorpyrifos oxon have the ability to prompt a variety of damaging effects on different body organs [ 1 , 3 , 5 ]. Due to the lipophilicity of CPF, the nervous system is a primary target for CPF; hence, it can facilely pass the blood–brain barrier and dismantle its stability, resulting in disruption of neuronal transmission and development of neurological disorders [ 5 , 6 ].…”