Agmatine alleviates brain oxidative stress induced by sodium azide

Abstract

Abstract Introduction: The brain is highly susceptible to oxidative damage due to excessive O2 tension, high concentration of oxidizable substrates, and low antioxidant capacity. Consequently, oxidative stress is linked to a number of brain disorders, and neurodegeneration. Sodium azide is a cytochrome oxidase inhibitor that promotes neurodegeneration by enhancing the release of excitotoxins and induces oxidative stress by peroxidation of membrane lipids, resulting in the release of intra-mitochondrial Ca + 2 and H2O2 (ROS Dependent-Ca + 2 release). Agmatine, a biogenic amine, is also referred to as a free radical scavenger and it protects the brain from membrane collapse, apoptosis, and mitochondrial swelling. The present study was designed to identify the antioxidative effects of agmatine on sodium azide-induced oxidative stress in brain tissues. Methodology: 24 male albino Wistar rats were divided into water and sodium azide (5 mg/kg-i.p) treated groups for 14 days. Animals were further divided for the following two weeks into water and agmatine (100 mg/Kg). Following the treatment of agmatine for an hour, all behaviors were recorded. Brain homogenates were used for biochemical estimations. Results: Agmatine-treated animals significantly increased (P < 0.01) their entry and time spent in the light box and open arms of the light/dark transition box and elevated plus maze tests, respectively. While agmatine treatment also increased (P < 0.01) the total number of squares crossed in the open field test. Agmatine also reduced (P < 0.01) the levels of reactive oxygen species and malondialdehyde whereas the antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), as well as antioxidant (glutathione) levels were significantly elevated (P < 0.01) in the animals treated with agmatine as compared with controls. Conclusion: The present study revealed that agmatine has substantial effects on oxidative and antioxidant enzyme levels in sodium azide-induced oxidative stress. While agmatine-treated rats determined decreased reactive oxygen species levels and improvement in behavioral impairments resulting from sodium azide administration.