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Volume 19, Issue 4 (October 2025)
IJT 2025, 19(4): 235-247 |
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Ethics code: UIL/FBMS/AN2113
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Imam A, Akinosho Akorede A, Ajibola O E, Oludare O J, 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) :235-247
URL: http://ijt.arakmu.ac.ir/article-1-1499-en.html
URL: http://ijt.arakmu.ac.ir/article-1-1499-en.html
Aminu Imam *1 
, Aalimah Akinosho Akorede2 , Oluwadamilola Eunice Ajibola3 , Oyeniyi Joseph Oludare3 , Micheal Olatunji Avoseh4 , Olanrewaju Ridwan Adeniyi3 , Moyosore Salihu Ajao3
, Aalimah Akinosho Akorede2 , Oluwadamilola Eunice Ajibola3 , Oyeniyi Joseph Oludare3 , Micheal Olatunji Avoseh4 , Olanrewaju Ridwan Adeniyi3 , Moyosore Salihu Ajao3
1- Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin 240003, Nigeria. , imam.a@unilorin.edu.ng
2- Department of Biological Sciences, Faculty of Arts and Sciences, DE 19711 University of Delaware, United States of AmericaIndonesia.
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.
2- Department of Biological Sciences, Faculty of Arts and Sciences, DE 19711 University of Delaware, United States of AmericaIndonesia.
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: (301 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 aimed to investigate the neurotoxic effects of DDVP, focusing on its oxido-inflammatory mechanisms and neurobehavioral implications. It also explored the potential therapeutic benefits of supplemental atropine and citric acid co-treatment.
Methods: Sixty-four male Wistar rats were divided into groups and treated with standard rat pellets and water ad libitum, DDVP alone, DDVP + atropine, DDVP + citric acid, or DDVP + atropine + citric acid. Neurobehavioral profiles were assessed, and biochemical analyses were conducted to evaluate oxidative stress, inflammatory markers, and neurotransmitter parameters.
Results: DDVP exposure significantly decreased cholinergic activity, increased oxidative stress and inflammatory neurochemicals, and resulted in poor neurobehavioral outcomes. 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: DDVP 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 may offer considerable therapeutic advantages in cases of organophosphate poisoning.
Methods: Sixty-four male Wistar rats were divided into groups and treated with standard rat pellets and water ad libitum, DDVP alone, DDVP + atropine, DDVP + citric acid, or DDVP + atropine + citric acid. Neurobehavioral profiles were assessed, and biochemical analyses were conducted to evaluate oxidative stress, inflammatory markers, and neurotransmitter parameters.
Results: DDVP exposure significantly decreased cholinergic activity, increased oxidative stress and inflammatory neurochemicals, and resulted in poor neurobehavioral outcomes. 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: DDVP 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 may offer considerable therapeutic advantages in cases of organophosphate poisoning.
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The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
