Abstract
CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs’ antioxidant, anti-inflammatory, and anti-apoptotic effects.
Highlights
Chlorpyrifos (CPF), (O,O-diethyl-O-(3,5,6-trichloro-2-pyridyl) phosphorothioate), is part of a wide range of chlorinated organophosphate insecticides that is ubiquitously applied around the world to combat agricultural and domestic insects [1,2,3]
CPF is an organophosphorus pesticide that is profoundly used to combat a variety of insects
AchE is a pivotal enzyme in the nervous system; wherefore, it is considered as a standard biomarker for organophosphateinduced neurotoxicity [36]
Summary
Chlorpyrifos (CPF), (O,O-diethyl-O-(3,5,6-trichloro-2-pyridyl) phosphorothioate), is part of a wide range of chlorinated organophosphate insecticides that is ubiquitously applied around the world to combat agricultural and domestic insects [1,2,3]. 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]. CPF has been reported to interfere with acetylcholinesterase (AchE) in central and peripheral nervous systems, allowing acetylcholine to accumulate in the synaptic cleft, resulting in uncontrolled cholinergic pathway activation and interrupting neuronal transmission [1,7]. A growing body of research proposes that massive creation of damaging reactive oxygen species (ROS) is another possible mechanism implicated in CPF-induced neurotoxicity [8,9,10]. CPF has been shown to enhance inflammatory responses by upregulating proinflammatory cytokines, especially tumor necrosis factor (TNF-α) and interleukin-1 (IL-1β) [9]
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