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Oxidative stress and apoptosis are markers in renal toxicity following Egyptian cobra (Naja haje) envenomation

This paper is available in a repository.
This paper is available in a repository.

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Abstract

Snakebite is a serious and important problem in tropical and subtropical countries including Egypt. The venom of Egyptian cobra (Naja haje; L.) is complex, and it has been considered as a good source of short neurotoxins and several cytotoxins. In this study, oxidative stress inductions as well as apoptotic effects of the Egyptian cobra crude venom at a dose of 0.025mg/kg (intraperitoneal injection; i.p.) has been investigated in kidney of rats after 4 h. Twelve rats divided into 2 groups, Group I served as control group, Group II received i.p. injection of 0.025mg/kg of crude venom. The venom enhanced lipid peroxidation and nitric oxide productions in the kidney with concomitant reduction in glutathione content and superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase activities were inhibited. Moreover, the venom induced a renal injury as indicated by histopathological changes in the kidney tissue with an elevation in serum creatinine and urea. In addition, the renal ultrastructural changes were in the form of blebbing of visceral epithelial cells, and foot process disorganization. Also, the glomerular capillaries lined by hypertrophied endothelial cells. These findings were associated with the pro-apoptotic action in the kidney. The results suggest that Egyptian cobra venom stimulates oxidative stress to induce apoptosis in renal tissue through inhibition of mitochondrial respiration in male rats.