Oxidative Stress in Wistar Rats Under Acute Restraint Stress and Its Modulation by Antioxidants and Nitric Oxide Modulators

Abstract

Background: Several pathogenic conditions leading to morbidity, including cancer, aging, diabetes, reperfusion injury, cardiovascular disease, and neurological disorders, are known to be exacerbated by oxidative stress. Antioxidant therapy is effective in the treatment of such disorders and appears to be a potential therapeutic technique to reduce oxidative stress. The aim of our study is to investigate the antioxidant effects of L-ascorbic acid and nitric oxide (NO) modulators on rats suffering from oxidative stress induced by acute restraint stress (RSx1). Methodology: In this in vivo study, Wistar rats were subjected to one hour of restraint stress on day 21 to induce oxidative stress. Superoxide dismutase (SOD), total antioxidant capacity (TAC), catalase, glutathione (GSH), and malondialdehyde (MDA) were used to assess the antioxidant effects. IBM Corp. Released 2013. IBM SPSS Statistics for Windows, Version 22.0. Armonk, NY: IBM Corp. was used for data analysis. Results: Compared to vehicle groups, acute restraint stress (RSx1) dramatically increased MDA levels while decreasing GSH, SOD, total antioxidant capacity, and catalase. L-NAME, 7-NI, AG (50 mg/kg each), and L-ascorbic acid (200 mg/kg) reversed the changes in SOD, MDA, GSH, total antioxidant capacity, and catalase levels. The NO precursor L-arginine (1000 mg/kg) and NO synthase inhibitors followed the same trend. Conclusion: Our study findings highlight the complex role of antioxidants and NO modulators in the pathogenesis of diseases, as evidenced by the reversal of oxidative stress indicators. Antioxidant therapy, with its potential to mitigate oxidative stress, emerges as a viable treatment option for a range of pathological conditions associated with oxidative stress.

Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation

“…Mammalian cells use redox reactions to generate energy and synthesize cellular components from nutrients. The main redox couples involved are nicotinamide adenine dinucleotide in its oxidized and reduced forms (NAD + /NADH), nicotinamide adenine dinucleotide phosphate in its oxidized and reduced forms (NADP + /NADPH), and GSH/GSH disulfide (GSSG) [31,32]. NAD + acts as an electron acceptor in glycolysis, whereas NADH donates electrons to mitochondrial OXPHOS.…”