Neuroprotective Effects of Curcumin Against Organophosphate-Induced Neurotoxicity in Wistar Rats: Mechanistic Insights

Organophosphate pesticides are widely used in Nigerian agriculture for crop protection and veterinary ectoparasite control, and unintended exposures represent a significant cause of toxicosis in livestock, companion animals, and wildlife. The primary mechanism of organophosphate toxicity involves irreversible acetylcholinesterase inhibition, leading to excessive cholinergic stimulation, oxidative stress, and neuronal apoptosis. Curcumin, the bioactive polyphenol from Curcuma longa, has demonstrated neuroprotective properties in several experimental models through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. This study investigated the neuroprotective effects of curcumin against sub-chronic oral dichlorvos-induced neurotoxicity in Wistar rats. Forty rats were allocated to five groups: vehicle control, dichlorvos alone at 5 mg/kg, dichlorvos plus curcumin at 100 mg/kg, dichlorvos plus curcumin at 200 mg/kg, and curcumin alone. All treatments were administered daily for 28 days. Endpoints included brain acetylcholinesterase activity, oxidative stress markers in brain tissue including malondialdehyde, superoxide dismutase, and catalase, neurological behavioural tests including open field and Morris water maze, and histopathological examination of brain sections. Dichlorvos significantly reduced acetylcholinesterase activity, elevated malondialdehyde, impaired spatial learning, and caused hippocampal neuronal degeneration. Curcumin co-treatment dose-dependently reversed these changes, with the 200 mg/kg dose restoring acetylcholinesterase activity to 78 percent of control values and significantly reducing hippocampal lesion scores. These mechanistic findings support curcumin as a promising adjunct neuroprotective agent in organophosphate toxicosis management relevant to Nigerian veterinary toxicology. Keywords: curcumin, organophosphate, neurotoxicity, acetylcholinesterase, neuroprotection.