The Effect of NO System on Ethidium Bromide-Induced Oxidative Stress in the Hippocampal Formation of Male Rats

 Acute and chronic effects of nitric oxide on oxidative stress and neuronal demyelination have been reported in human and animal models. 

 Oxidative stress is involved in the pathogenesis of demyelinated animals; thus, this study investigated the effects of nitric oxide system and ethidium bromide on oxidative stress in the hippocampal formation.  

 This experimental study was performed on eight groups of male rats, as follows: control, control, ethidium bromide, L-Arginine, L-NAME, ethidium bromide + L-Arginine, ethidium bromide + L-NAME, and ethidium bromide + L-Arginine + L - NAME. Three days after the injection of drugs into the hippocampal CA1 area, hippocampal biopsy was performed, and oxidative stress parameters were measured in this area. One-way analysis of variance (ANOVA) and posthoc tests were used for data analysis.

 Injection of 3 μL ethidium bromide into the CA1 region increased oxidative stress parameters (P<0.01). Injection of 15.3 μg/rat L-Arginine in this region stopped the response of ethidium bromide (P<0.05, P<0.01); while, the injection of 15.1 μg/rat L-NAME failed to return the effects of the ethidium bromide. Moreover, the combination of 15.3 μg/rat L-Arginine and 15.1 μg/rat L-NAME only returned lipid peroxidation caused by the injection of 3 μL of ethidium bromide to normal (P<0.05); this process failed to improve antioxidant enzymes.

 The obtained results suggested the excitatory effect of the nitric oxide system on alleviating oxidative stress induced by ethidium bromide in the CA1 region of male rats.