Ethics code: UIL/FBMS/AN2113
Imam A, Akinosho Akorede A, Ajibola O E, Oyeniyi J O, Avoseh M O, Adeniyi O R et al . Synergistic Neuroprotection Effects of Atropine and Citric Acid Mitigate Dichlorvos-Induced Neurotoxicity and Oxidative Stress. IJT 2025; 19 (4)
URL:
http://ijt.arakmu.ac.ir/article-1-1499-en.html
1- Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin 240003, Nigeria , imam.a@unilorin.edu.ng
2- Faculty of Arts and Sciences, Department of Biological Sciences, DE 19711 University of Delaware, United States of America
3- Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin 240003, Nigeria
4- Department of Biology, Illinois State University, IL61761, United States of America
Abstract: (19 Views)
Background: Dichlorvos (DDVP), an organophosphate, inhibits acetylcholinesterase, leading to acetylcholine accumulation and subsequent muscarinic receptor hyperstimulation. This disrupts normal electrochemical impulse transmission and redox homeostasis. Atropine, a competitive muscarinic receptor antagonist, is the primary antidote for organophosphate poisoning, mitigating muscarinic hyperstimulation. Concurrently, citric acid is recognized for its antioxidant properties and potential to combat oxidative stress. This study investigated the neurotoxic effects of dichlorvos, focusing on its oxido-inflammatory mechanisms and neurobehavioral implications. We also explored the potential therapeutic benefits of supplemental atropine and citric acid co-treatment. Materials and Methods: Sixty-four male Wistar rats were divided into groups and treated with: standard rat pellets and water ad libitum, dichlorvos alone, dichlorvos + atropine, dichlorvos + citric acid, or dichlorvos + atropine + citric acid. Neurobehavioral profiles were assessed, and biochemical analyses were conducted to evaluate oxidative stress, inflammatory markers, and neurotransmitter parameters. Results: Dichlorvos exposure significantly decreased cholinergic activity, increased oxidative stress and inflammatory neurochemicals, and resulted in poor neurobehavioral outcomes. Most of these detrimental effects were stabilized by co-treatment with citric acid and atropine. The antioxidant and anti-inflammatory capacities of citric acid significantly supplemented atropine's neuroprotective mechanisms, potentially preventing long-term sequelae.
Conclusion: Dichlorvos ingestion leads to significant neurobehavioral dysfunction by disrupting cholinergic, monoaminergic, and oxido-inflammatory functions. Supplementation with atropine and citric acid markedly improved neurobehavioral outcomes, largely attributed to the neuroprotective effects of citric acid. These findings suggest that antioxidant supplementation in organophosphate poisoning may offer considerable therapeutic advantages.
Type of Study:
Research |
Subject:
General