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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). 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. 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.

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