The Role of Vitamin C in Vanadyl-Sulfate-Induced Nephrotoxicity and Hepatotoxicity

Vanadium (V) is a candidate to decrease the serum level of glucose in diabetic animal model. However, it affects the lipid peroxidation and antioxidant activity so could make nephrotoxicity and hepatotoxicity. In this study, the protective role of vitamin C as an antioxidant on nephrotoxicity and hepatotoxicity induced by vanadyl sulfate was investigated. This study was designed in 2 protocols. There were 3 groups in protocol 1 that received saline (group 1), saline daily for 7 days plus single dose of vanadyl sulfate (50 mg/kg intraperitoneally) in day 2 (group 2), or vitamin C (250 mg/kg intraperitoneally) daily for 7 days and single dose of vanadyl sulfate (group 3). There were 2 groups in protocol 2 that received saline plus single dose of vanadyl sulfate (50 mg/kg intraperitoneally) in day 2 (group 4) or vitamin C (250 mg/kg intraperitoneally) daily for 2 days plus single dose of vanadyl sulfate (group 5). At the end of experiment, blood samples were collected to measure serum level of blood urea nitrogen (BUN), creatinine (Cr), aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP), and all animals were sacrificed for histopathology investigation and determination of kidney tissue damage score (KTDS). In protocol 1, BUN/Cr ratio, kidney weight (KW), and KTDS decreased significantly in vanadyl sulfate plus vitamin C group in comparison with vanadyl sulfate plus saline group (P < 0.05). In addition, serum level of AST and ALP significantly decreased in vanadyl sulfate plus vitamin C group. In protocol 2, not only similar results were not observed, but also vitamin C increased the side effects of vanadyl sulfate. Administration of vitamin C as a potent antioxidant could decrease the vanadium-induced toxicity. So, as vanadyl sulfate can be used for diabetic model in laboratory, vitamin C can be useful to decrease the vanadium-induced nephrotoxicity and hepatotoxicity, too.