Zinc and ascorbic acid treatment alleviates systemic inflammation and gastrointestinal and renal oxidative stress induced by sodium azide in rats

Abstract

Background: Sodium azide (NaN3) is a chemical of rapidly increasing economic importance but with high toxic attributes. In this study, the effects of zinc (Zn) and ascorbic acid (AsA) supplementation on sodium azide (NaN3) - induced toxicity in the stomach, colon and kidneys were evaluated in Wistar rats. Twenty-eight rats were randomly allocated to four experimental groups as follows: group A (control) given distilled water only; group B (NaN3 only, 20 mg/kg); group C (NaN3 + zinc sulphate, ZnSO4 80 mg/kg); and group D (NaN3 + AsA 200 mg/kg). Results: NaN3 was found to significantly (p < 0.05) induce increases in serum nitric oxide (NO), advanced oxidation protein products (AOPP), myeloperoxidase (MPO) and total protein levels, along with significant (p < 0.05) increase in gastric, colonic and renal malondialdehyde (MDA) and protein carbonyl (PCO) levels. In addition, NaN3 induced significant (p < 0.05) reduction in superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities in the colon and kidneys. Treatment with Zn or AsA caused significant (p < 0.05) reduction in serum levels of oxidative and inflammatory markers, as well as tissue PCO and MDA levels. Moreover, co-treatment with Zn or AsA significantly (p < 0.05) restored colonic and renal levels of antioxidant enzymes, reduced glutathione and protein thiols. Conclusions: This study shows that Zn or AsA supplementation alleviated NaN3 toxicity by suppressing systemic inflammation and preventing oxidative damage in the stomach, colon and kidneys of rats.