Research Article Hemin Attenuates Cisplatin-Induced Acute Renal Injury in Male Rats Mohamed A. Al-Kahtani, 1 Ashraf M. Abdel-Moneim, 1,2 Omar M. Elmenshawy, 1,3 and Mohamed A. El-Kersh 4,5 1 Department of Biological Sciences, Faculty of Science, King Faisal University, Al-Hassa 31982, Saudi Arabia 2 Department of Zoology, Faculty of Science, Alexandria University, Alexandria 21511, Egypt 3 Department of Zoology, Faculty of Science, Al-Azhar University, Nasr City 11884, Egypt 4 Department of Chemistry, Faculty of Science, King Faisal University, Al-Hassa 31982, Saudi Arabia 5 Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria 21511, Egypt Correspondence should be addressed to Mohamed A. Al-Kahtani; malkahtani@kfu.edu.sa and Ashraf M. Abdel-Moneim; aabdelmoneim@kfu.edu.sa Received 11 May 2014; Revised 30 July 2014; Accepted 6 September 2014; Published 22 September 2014 Academic Editor: Madia Trujillo Copyright © 2014 Mohamed A. Al-Kahtani et al. his 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. Background. he aim of this study is to investigate the protective efects of hemin (the heme oxygenase-1 [OH-1] inducer) against nephrotoxic efects induced by cisplatin [cis-diamminedichloroplatinum II (CP)] in male rats. Methods. he evaluation was performed through monitoring renal redox parameters: lipid peroxidation (LPO), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR), and reduced glutathione (GSH). he work also examined renal function tests (urea and creatinine), tissue proinlammatory mediator like nitric oxide (NO), and kidney cytopathology. Results. A single intraperitoneal dose of CP (10 mg/kg b.w.) caused signiicant elevation of blood urea, serum creatinine, and renal LPO and NO, along with signiicant decline of the activities of GPx and GR, but renal SOD activity and GSH level were statistically insigniicant as compared to control group. Subcutaneous injection of hemin (40 mol/kg b.w.) partially ameliorated CP-induced renal damage, based on suppression of blood urea, serum creatinine, the renal MDA and NO levels, and increased antioxidant capacity in CP-treated rats. he results of histopathological and ultrastructural investigations supported the renoprotective efect of hemin against CP-induced acute toxicity. Conclusion. he induction of HO-1 by hemin is a promising approach in the treatment of CP-induced nephrotoxicity. However, further preclinical studies are warranted to test efectiveness of CP/hemin on the outcome of tumor chemotherapy. 1. Introduction Cisplatin (cis-diamminedichloroplatinum(II), CP) is a highly efective chemotherapeutic agent against a large spectrum of tumor types [1–3]. However, the long-term clinical use of CP is limited by its serious side efects, mainly nephrotoxicity [4]. CP causes impairment of kidney function and acute renal failure via multiple mechanisms including generation of oxygen/nitrogen species, DNA damage, tubulointerstitial inlammation, and apoptotic cell death [5–12]. A number of studies have evaluated compounds as potential nephro- protectors against CP; these included natural antioxidants, modulators of nitric oxide synthesis, osmotic diuretics, and cytoprotective and antiapoptotic agents [13]. However, most of them were not found suitable/safe for clinical practice. In this context, heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, might ofer a promising alterna- tive. HO-1 (also known as heat shock protein 32) is induced by free radical-initiated reactions, and its induction is con- sidered to be an adaptive response against oxidative tissue damage [14–20]. In addition, HO-1 has been recognized to exhibit powerful anti-inlammatory and immunomodulatory efects [21]. Previous studies have shown that HO-1-inducing agents, as hemin, can mitigate nephrotoxic efects caused by a wide array of stressors, including mercury [15] and acetaminophen [20]. Based on the previous information, the present study aimed to examine whether the activation of HO-1 (by hemin) would have protective efects against CP Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 476430, 9 pages http://dx.doi.org/10.1155/2014/476430