Research Article Phenolic Acids (Gallic and Tannic Acids) Modulate Antioxidant Status and Cisplatin Induced Nephrotoxicity in Rats Seun F. Akomolafe, 1 Ayodele J. Akinyemi, 2 and Scholarstical O. Anadozie 2 1 Department of Biochemistry, Ekiti State University, P.M.B 5363, Ado Ekiti, Nigeria 2 Department of Biochemistry, Afe Babalola University, P.M.B 5454, Ado Ekiti, Nigeria Correspondence should be addressed to Seun F. Akomolafe; purposefulseun@yahoo.co.uk Received 21 March 2014; Revised 21 May 2014; Accepted 2 June 2014; Published 11 August 2014 Academic Editor: Ottavio Giampietro Copyright © 2014 Seun F. Akomolafe et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cisplatin (cis-diamminedichloroplatinum (II) or CDDP), used in the treatment of many solid-tissue cancers, has its chief side- effect in nephrotoxicity. Hence, this study sought to investigate and compare the protective effect of gallic acid (GA) and tannic acid (TA) against cisplatin induced nephrotoxicity in rats. e rats were given a prophylactic treatment of GA and TA orally at a dose of 20 and 40mg/kg body weight for 7 consecutive days before the administration of a single intraperitoneal (i.p.) injection of cisplatin (CP) at 7.5mg/kg bwt. e protective effects of both GA and TA on CP induced nephrotoxicity were investigated by assaying renal function, oxidative stress biomarkers, and histopathological examination of kidney architecture. A single dose of cisplatin (7.5 mg/kg bwt) injected i.p. caused a significant increase in some biomarkers of renal function (creatinine, uric acid, and urea levels), with a marked elevation in malondialdehyde (MDA) content accompanied by a significant ( < 0.05) decrease in reduced glutathione (GSH) content (103.27%) of kidney tissue as compared to control group. Furthermore, a significant ( < 0.05) reduction in kidney antioxidant enzymes (SOD, catalase, GPx, and GST) activity was observed. However, pretreatment with oral administration of tannic acid and gallic acid at a dose of 20 and 40mg/kg body weight, respectively, for 7 days prior to cisplatin administration reduced histological renal damage and suppressed the generation of ROS, lipid peroxidation, and oxidative stress in kidney tissues. ese results indicate that both gallic and tannic acids could serve as a preventive strategy against cisplatin induced nephrotoxicity. 1. Introduction e use of chemotherapy in the treatment of cancer has opened new possibilities for improvement of the quality of life of cancer patients. Despite its success, treatment with some of the most effective anticancer drugs shows a number of symp- toms of direct toxicity [1]. In recent years, the mechanism of cisplatin (cis-diamminedichloroplatinum (II) or CDDP) induced nephrotoxicity has gradually been elucidated [2]. Studies have shown an increase in lipid peroxides in the renal tissue of CDDP-administered animals [3], a decrease in reduced glutathione levels [1], and the induction of metallothionein [4], an antioxidant. ese changes have been considered to result from the generation of reactive oxygen species (ROS). Studies using chemiluminescence or electron spin resonance (ESR) have shown that CDDP generates OH radical [5, 6]. Nephrotoxicity involves kidney damage or dysfunction arising from direct or indirect exposure to drugs and industrial or environmental chemicals. Cisplatin ((cis- diamminedichloroplatinum (II) or CDDP)), an anti- neoplastic drug have been reported to induce nephrotoxicity [7]. e kidney which is the major route of cisplatin excretion also accumulates it to a greater degree than other organs [6, 8]. Oxidative stress, inflammation, and apoptosis are some of the mechanisms already established to explain cisplatin induced acute kidney injury [9]. A number of strategies have been proposed for the prevention/management of cisplatin induced nephrotoxicity, since there is no specific treatment, with the use of some synthetic drugs which have been Hindawi Publishing Corporation International Scholarly Research Notices Volume 2014, Article ID 984709, 8 pages http://dx.doi.org/10.1155/2014/984709