%0 Journal Article
%T Vitamin E Is a Nephroprotectant Agent in Male but Not in Female in a Model of Cisplatin-Induced Nephrotoxicity
%A Sima Jilanchi
%A Mehdi Nematbakhsh
%A Mehrnoosh Bahadorani
%A Ardeshir Talebi
%A Fatemeh Eshraghi-Jazi
%A Azam Mansouri
%A Farzaneh Ashrafi
%J ISRN Nephrology
%D 2013
%R 10.5402/2013/280395
%X Background. The role of gender for nephroprotectant agent such as vitamin E in cisplatin- (CP-) induced nephrotoxicity has not been documented yet. Methods. One group from each gender of Wistar rats received a single dose of CP (7£¿mg/kg; i.p) and was treated with vitamin E (1£¿g/kg/day) for 7 days, and they were compared with similar gender in the control group. Results. The serum levels of blood urea nitrogen (BUN) and creatinine (Cr) in male animals treated with CP was not different from the control group, but it was significantly different in the female rats ( ). The CP-induced damage intensity in male kidney tissue was not significantly different between the CP-treated and control groups, but this was not the case in female, indicating that the tissue damage in female is significantly different from the control group ( ). No significant difference in serum levels of magnesium (Mg), nitrite, malondialdehyde (MDA), and lactate dehydrogenase (LDH) was seen between the genders. Kidney weight and body weight changes were statistically significant in both genders ( ). Significant difference was observed in uterus weight between the two groups of female ( ). Conclusion. Vitamin E may prevent CP-induced nephrotoxicity in male, but possibly it has not such nephroprotectant effect in female. 1. Introduction Cisplatin (CP) is an antitumor drug widely used in clinic [1]. This drug contains heavy metal platinum [2] and is used to treat a variety of neoplasms such as head, neck, testicular, ovarian, bladder, small cell lung, and esophagus cancers [3]. CP therapy produces free radicals such as superoxide and hydroxyl [4, 5] that lead to oxidative stress followed by nephrotoxicity, neurotoxicity, hepatotoxicity [2, 6], and endothelial dysfunction [7, 8]. Kidney dysfunction causes glutathione depletion [9], decreases creatinine (Cr) clearance [10], and decreases the glomerular filtration rate [11, 12]. To prevent CP-induced nephrotoxicity, renin angiotensin receptor antagonist (losartan) and different antioxidant substances have been suggested to be supplemented. L-arginine is the main precursor of nitric oxide (NO) in vascular endothelium, and its renoprotection role against CP-induced nephrotoxicity was reported [13]. The effects of vitamins C and E on renal injury induced by CP have been reported previously. Vitamin C reduces free radicals in many biological processes [14] and protects the kidney against CP-induced oxidative stress [14]. Vitamin E, as a membrane stabilizer, is well known as free radical scavenger [15], and its nephroprotective role against
%U http://www.hindawi.com/journals/isrn.nephrology/2013/280395/