Effects of Quercetin and Chrysin on 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induced Hepatotoxicity in Rats Osman Ciftci, 1 Nigar Vardi, 2 Ilknur Ozdemir 3 1 Faculty of Pharmacy, Department of Pharmaceutical Toxicology, University of Inonu, 44 280, Malatya, Turkey 2 Faculty of Medicine, Department of Histology and Embryology, University of Inonu, 44 280, Malatya, Turkey 3 Faculty of Science and Arts, Department of Biochemistry, University of Inonu, 44 280, Malatya, Turkey Received 15 December 2010; accepted 4 February 2011 ABSTRACT: The objective of current study is to investigate the effects of the administration of chrysin (CH) and quercetin (Q) on rat liver in which oxidative and histological damage had been induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Rats were randomly divided into six equal groups. TCDD was orally administered at the dose of 2 lg/kg/week, and Q and CH were orally administered at the doses of 20 mg/kg day and 50 mg/kg/day, respectively, by gavages dissolved in corn oil. The liver samples to be analyzed for the determination of oxidative and histological alternations were taken from rats at 60 days. The results indicated that although 2,3,7,8-TCDD significantly induced (P  0.01) lipid peroxidation (increase of MDA levels), it positively affected oxidant/antioxidant system (a decline in the levels of GSH, CAT, GSH-Px, and CuZn-SOD) in rats significantly. The histological changes observed in the liver corre- lated with the biochemical findings. However, these effects of TCDD on oxidative and histological changes were eliminated by Q and CH treatment. In conclusion, TCDD caused an adverse effect on rat’s liver. When Q and CH were given together with TCDD, they prevented hepatotoxicty induced by TCDD. Thus, it is thought that Q and CH may be useful as a new category of anti-TCDD toxicity agent. # 2011 Wiley Periodi- cals, Inc. Environ Toxicol 00: 000–000, 2011. Keywords: 2,3,7,8-TCDD; quercetin; chrysin; hepatotoxicity INTRODUCTION 2,3,7,8-Tetracholorodibenzo-p-dioxin (TCDD) is a ubiqui- tous environmental contaminant which produces some adverse and biochemical effects in experimental animals (Alsharif and Hassoun, 2004; Hassoun et al., 2004). Much of the concern with exposure to TCDD is due to their envi- ronmental and biological persistence, which may result in the bioconcentration and bioaccumulation of the chemicals up to the food chain (Guo et al., 2001). In experimental animals and humans, TCDD causes a variety of toxic responses including wasting syndrome, hepatotoxicity, immunotoxicity, teratogenicity, mutagenesis, and carcino- genesis (Hassoun et al., 2004; Ciftci et al., 2010). The relative potencies of TCDD are related to their binding affinities to the aryl hydrocarbon receptor (AhR). Besides, oxidative stress is an important constituent in the mecha- nism of TCDD toxicity (Slezak et al., 2000; Hassoun et al., 2004). It has been shown that TCDD enhances lipid Correspondence to: O. Ciftci; e-mail: ociftci@inonu.edu.tr Contract grant sponsor: IUBAP (Scientific Research Fund of Inonu University) Contract grant number: 2009/24 Published online in Wiley Online Library (wileyonlinelibrary.com). DOI 10.1002/tox.20707  C 2011 Wiley Periodicals, Inc. 1