Vitamin E protection against gentamicin-induced nephrotoxicity in rats: a biochemical and histopathologic study

Document Type : Full paper (Original article)

Authors

1 Department of Pathobiology, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran

2 Graduated from Faculty of Veterinary Medicine, Islamic Azad University of Kazeroun, Kazeroun, Iran

3 Graduated from Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran

Abstract

The specificity of gentamicin for vitamin E deficiency-associated oxidative stresses in the renal proximal convoluted tubules is apparently related to its ability to increasingly facilitate generation of radical species in mitochondria. To determine the ways in which vitamin E manage the currently processes, we conducted a prospective study aimed to investigate the tubular preserving effect of vitamin E, pre-treatment and cotreatment, in nephrotoxicity with gentamicin-treated Sprague-Dawley rats. 35 healthy rats were ascribed 1–5 trials to receive once daily intramuscular injections of either gentamicin (80 mg/kg/body Wt) (GN), normal saline (NS), vitamin E (250 mg/kg/body Wt) (VE), vitamin E (250 mg/kg/body Wt) plus gentamicin (80 mg/kg/body Wt) simultaneously (CGE), or vitamin E alone (250 mg/kg/body Wt) 3 days before coadministration with gentamicin (80 mg/kg/body Wt) (PGE), for 10 days. Gentamicin alone caused a decrease in glomerular filtration rate-associated coefficient of the creatinine clearance, increase in blood content of BUN as well as a decrease in tubular function evident by recognised depression of ATPase activity, increases in lipid peroxidation and subsequently MDA activity. The histopathologic studies revealed acute tubular necrosis with tubular cast formation triggered by gentamicin treatment over 10 days of experiment and change in size and pattern of tubules. Further biochemical studies showed tubular preserving effect of vitamin E pre-administration including slow down in rising enzyme activity (MDA) and mild to moderate BUN with recovery in creatinine clearance and holding ATPase activity up to 50% on comparison with the control and vitamin E alone-treated rats. Significant tubular resistance against gentamicin proximal tubular lesions on the suppressed activity of lipid oxidation induced by vitamin E pre-treatment with normal size during microscopic inspections lead us to conclude protective role of vitamin E is probably attributed to tubular prevention, whereas hyperemia prepared by vitamin is only a consequent.

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