Protective effect of captopril against diazinon induced nephrotoxicity and neurotoxicity via inhibition of ROS-NO pathway

Abstract

Diazinon (Dz) is a widely used insecticide. It can induce nephrotoxicity and neurotoxicity via oxidative stress. Captopril, an angiotensin-converting enzyme inhibitor, is known for its antioxidant properties. In this study, we used captopril for ameliorating of Dz-induced kidney and brain toxicity in rats. Animals were divided into five groups as follows: negative control (olive oil), Dz (150 mg kg), captopril (60 and 100 mg kg) and positive control (N-acetylcysteine 200 mg kg) were injected intraperitoneally 30 min before Dz. After 24 h, animals were anesthetized and the brain and kidney tissues were separated. Then oxidative stress factors were evaluated. Also, blood was collected for assessment of blood urea nitrogen (BUN), creatinine (Cr) and nitric oxide (NO) levels. Dz significantly increased oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation, and protein carbonyl as well as glutathione (GSH) oxidation in both tissues. Increased levels of the BUN, Cr and NO were observed after Dz injection. Interestingly, captopril administration significantly decreased ROS production in both tissues. Captopril significantly protected kidney and brain against lipid peroxidation and GSH oxidation. Administration of captopril could markedly inhibit protein carbonyl production in kidney and brain after Dz injection. Furthermore, captopril ameliorated the increased level of BUN, Cr and NO. These results suggested that captopril can prevent Dz-induced oxidative stress, nephrotoxicity and neurotoxicity because of its antioxidant activity.

Mitochondrial toxicity of aluminium nanoparticles in comparison to its ionic form on isolated rat brain mitochondria

“…The ROS level was measured using dichlorofl uorescin-diacetate (DCFH-DA) through a Shimadzu RF5000U fl uorescence spectrophotometer at 485 nm excitation and 520 nm emission wavelength (18) .…”

Sulforaphane alleviates methamphetamine-induced oxidative damage and apoptosis via the Nrf2-mediated pathwayin vitroandin vivo

“…The overproduction of ROS and NO beyond the antioxidant capacity of cells could cause irrevocable severe oxidative damage to the cells post METH administration (Solhi et al, 2014;Wells et al, 2016). The excessive production of ROS also induces neuronal DNA damage that eventually leads to neurotoxicity (Pamies et al, 2018;Vahidirad et al, 2018). The increased percentage of the DNA tail and γH2AX represented the hallmarks for the detection of DNA damage (Chan et al, 2016).…”

Effect of Captopril on Brain Oxidative Damage in Pentylenetetrazole-Induced Seizures in Mice<br />

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