Research Article Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats Isaac A. Adedara, Amos O. Abolaji, Blessing E. Odion, Isioma J. Okwudi, Abiola A. Omoloja, and Ebenezer O. Farombi Drug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, Nigeria Correspondence should be addressed to Isaac A. Adedara; dedac2001@yahoo.co.uk Received 30 July 2014; Revised 28 September 2014; Accepted 28 September 2014; Published 15 October 2014 Academic Editor: M. Firoze Khan Copyright © 2014 Isaac A. Adedara 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. 2,5-Hexanedione (2,5-HD) is the toxic metabolite of n-hexane which is widely used as solvent in numerous industries. he present study elucidated the precise mechanism of 2,5-HD in hepatorenal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were exposed to 0, 0.25, 0.5, and 1% 2,5-HD in drinking water for 21 days. Exposure to 2,5-HD caused liver and kidney atrophy evidenced by signiicant elevation in serum aminotransferases, alkaline phosphatase, albumin, bilirubin, urea, creatinine, and electrolytes levels compared with control. he marked dose-dependent increase in total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) was accompanied with signiicant decrease in high-density lipoprotein (HDL) levels in 2,5-HD-exposed animals when compared with the control. Administration of 2,5-HD signiicantly diminished glutathione (GSH) level but increased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S- transferase (GST) concomitantly with marked elevation in hydrogen peroxide (H 2 O 2 ) and malondialdehyde (MDA) levels in liver and kidney of the treated groups compared with control. hese indings suggest that undue exposure to 2,5-HD at environmentally relevant levels may impair liver and kidney functions through induction of oxidative stress. 1. Introduction 2,5-Hexanedione (2,5-HD) is the main toxic metabolite of n-hexane, an organic solvent widely used in chemical engi- neering and pharmaceutical and cosmetic industries [1]. Previous toxicological studies have shown that n-hexane and its metabolites, 2,5-HD and 2-hexanone, were detected in the liver, kidney, brain, blood, and the developing fetus at time points up to 18 hours ater exposure [2]. 2,5-HD is known to cause testicular dysfunction, neurotoxicity, and genotoxicity and it adversely afects liver and kidney function in animals and humans [3–6]. An uncontrolled exposure to toxic indus- trial solvents is capable of causing biological damage which eventually could lead to pathological conditions and organ damage [7]. here is a growing concern over the safety of 2,5- HD exposure in humans. Epidemiological studies have been reported on n-hexane toxicity in Taiwan and China [1, 8]. However, relatively little is known about the mechanism of 2,5-HD toxicity to the liver and kidney. he adverse efects resulting from exposure to xenobiotics could occur via several mechanisms leading to signiicant alterations in the levels of biomolecules such as enzymes and metabolic products, normal functioning, and histomorphol- ogy of the organs. he paucity of information in the literature about 2,5-HD-induced hepatorenal toxicity accentuates the need to undertake a detailed study evaluating the antioxidant status of the kidney and liver in rats exposed to 2,5-HD. It is well known that oxidative stress is involved in the patho- genesis of several diseases following exposure to environ- mental contaminants. he liver is particularly vulnerable to toxicity produced by reactive metabolite because it is the major site of xenobiotic metabolism. he kidney is a highly specialized organ that maintains the internal environment of the body by selectively excreting or retaining various substances according to speciic body needs [9]. he ability of the kidney to concentrate the tubular luid by removing water and salts, consequently, predisposes the kidney to toxic chemicals. he biotransformation of chemicals to reactive Hindawi Publishing Corporation Journal of Toxicology Volume 2014, Article ID 239240, 9 pages http://dx.doi.org/10.1155/2014/239240