Royal Dental College

Carbofuran, a widely used N-methyl carbamate pesticide, induces acute cholinergic toxicity and long-term neurotoxicity through acetylcholinesterase inhibition, oxidative stress, and mitochondrial dysfunction. These mechanisms contribute to neurobehavioral impairments and systemic toxicity, posing significant public health concerns. This review aims to elucidate the mechanistic insights of carbofuran neurotoxicity and evaluate the potential neuroprotective effects of curcumin, a natural antioxidant compound, highlighting translational prospects for mitigating pesticide-induced neuronal damage. A comprehensive literature survey was conducted focusing on carbofuran’s toxicodynamic, oxidative and mitochondrial injury pathways, and preclinical and clinical evidence supporting curcumin’s antioxidant, anti-inflammatory, and mitochondrial stabilizing actions in models of pesticide toxicity. Carbofuran toxicity involves reversible carbamylation of acetylcholinesterase, excessive reactive oxygen species generation, lipid peroxidation, TCA cycle disruption, and endocrine axis interference. Curcumin demonstrates neuroprotection by scavenging ROS, modulating NF-κB signaling, restoring antioxidant enzyme activities, and improving mitochondrial function. Novel curcumin formulations improve bioavailability and efficacy against carbofuran-induced neurotoxicity in animal models. Curcumin presents a mechanistically promising neuro-nutraceutical candidate for attenuating carbofuran-induced neurotoxicity. However, challenges such as limited bioavailability and scarce clinical trials necessitate further research. Public health strategies should emphasize exposure prevention alongside exploring adjunct nutraceutical therapies.