Volume 28, Issue 165 (10-2018)
J Mazandaran Univ Med Sci 2018, 28(165): 175-182 |
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Vahidirad M, Arab-Nozari M, Mohammadi H, Shaki F. Protective Effect of Edaravone against Nephrotoxicity and Neurotoxicity of Acute Exposure to Diazinon. J Mazandaran Univ Med Sci 2018; 28 (165) :175-182
URL: http://jmums.mazums.ac.ir/article-1-10307-en.html
URL: http://jmums.mazums.ac.ir/article-1-10307-en.html
Abstract: (4233 Views)
Background and purpose: Diazinon (Dz) is a widely used insecticide. It can cause nephrotoxicity and neurotoxicity by induction of oxidative stress. Edaravone is a drug with antioxidant effect that is used in treatment of acute infraction disorders. In this study we used edaravone for ameliorating diazinon induced kidney and brain damage.
Materials and methods: Twenty four male Wistar rats were divided into the following groups: Control (normal saline), Dz (150mg/kg) and edaravone (10mg/kg and 20mg/kg) that were injected 30min before Dz. After 24 hr, the animals were anesthetized and the brain and kidney tissues were separated. Then oxidative stress factors were evaluated. Blood serum samples were also taken to determine the levels of BUN, creatinine, and nitric oxide.
Results: Dz significantly increased oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation, protein carbonyl, and glutathione oxidation in kidney and brain tissues. Also, the levels of BUN, creatinine and nitric oxide increased after Dz injection. Interestingly, ederavone administration significantly decreased ROS production in rats’ kidney and brain tissues (p<0.05). It also significantly protected kidney and brain against lipid peroxidation and glutathione oxidation (p<0.05). Edaravone treatment could noticeably inhibit diazinon induced protein carbonyl production in both tissues. Furthermore, edaravone significantly ameliorated the increased levels of BUN, creatinine, and nitric oxide due to Dz administration (p<0.05).
Conclusion: These data suggested that edaravone can prevent nephrotoxicity, neurotoxicity and acute toxicity of diazinon via reducing oxidative stress.
Materials and methods: Twenty four male Wistar rats were divided into the following groups: Control (normal saline), Dz (150mg/kg) and edaravone (10mg/kg and 20mg/kg) that were injected 30min before Dz. After 24 hr, the animals were anesthetized and the brain and kidney tissues were separated. Then oxidative stress factors were evaluated. Blood serum samples were also taken to determine the levels of BUN, creatinine, and nitric oxide.
Results: Dz significantly increased oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation, protein carbonyl, and glutathione oxidation in kidney and brain tissues. Also, the levels of BUN, creatinine and nitric oxide increased after Dz injection. Interestingly, ederavone administration significantly decreased ROS production in rats’ kidney and brain tissues (p<0.05). It also significantly protected kidney and brain against lipid peroxidation and glutathione oxidation (p<0.05). Edaravone treatment could noticeably inhibit diazinon induced protein carbonyl production in both tissues. Furthermore, edaravone significantly ameliorated the increased levels of BUN, creatinine, and nitric oxide due to Dz administration (p<0.05).
Conclusion: These data suggested that edaravone can prevent nephrotoxicity, neurotoxicity and acute toxicity of diazinon via reducing oxidative stress.
Type of Study: Brief Report |
Subject:
Pharmacy
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