*Corresponding author, e-mail: fguzun@gazi.edu.tr GU J Sci 31(2): 399-406 (2018) Gazi University Journal of Science http://dergipark.gov.tr/gujs Morin and Hesperidin Ameliorate Cisplatin-Induced Hepatotoxicity and Nephrotoxicity in Rats: A Histopathological Study Fatma Gökçe APAYDIN 1* , Kaan KALTALIOGLU 2 , Barbaros BALABANLI 1 , Şule COŞKUN-CEVHER 1 1 Gazi University, Department of Biology, 06500, Ankara-Turkey 2 Giresun University, Espiye Vocational School, Giresun, Turkey Article Info Abstract In this study, we investigated that the histopathological changes of rat kidney and liver tissues after cisplatin administration and potential beneficial effects of morin and hesperidin administration. Wistar rats were randomly divided in 7 groups: control, morin (M), hesperidin (H), cisplatin (CP), cisplatin+morin (CP+M), cisplatin+hesperidin (CP+H), cisplatin+morin+hesperidin (CP+M+H). Kidney and liver tissues were collected at the end of the experiment and were evaluated histopathological changes. Various histopathological changes in kidney and liver tissues of cisplatin-induced group were revealed. However, pre- and co-treatment of morin and/or hesperidin partially prevented these hepatotoxic and nephrotoxic changes in cisplatin-induced groups. Received: 08/09/2017 Accepted: 14/03/2018 Keywords Cisplatin Hepatotoxicity Hesperidin Histopathology Morin Nephrotoxicity 1. INTRODUCTION Cisplatin (CP, cis-diamminedichloroplatinum II) is using for antineoplastic drug in the treatment of cancer however in the previous studies researchers reported that cisplatin caused many toxic effects [1,2]. It is known that CP is a cytotoxic agent, and their cytotoxic effect is probably via its interaction with DNA that the formation of covalent adducts between certain DNA bases [3,4]. Nasr (2014) was showed that CP caused hepatotoxic effects on male rats when it was given 7,5 mg/kg i.p to rats. And it also through the alterations of liver biomarkers, lipid peroxidation biomarker (Malondialdehyde, MDA), antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and Glutathione-S-transferase (GSH) and histological parameters [3]. Some authors showed that CP has accumulative effect on some organs like kidney and liver [5]. CP elicits number of toxic effects including vestibular toxicity [6], reproductive toxicity [7,8], cardiotoxicity [9], hepatic dysfunction [3], teratogenic effect [10]. In previous studies, it is reported that CP causes oxidative stress [11]. The cells have different mechanisms to alleviate oxidative stress which is offered by enzymatic and non-enzymatic antioxidants. Antioxidants have been shown to scavenge reactive oxygen species (ROS) [12-14]. Studies have demonstrated that exposure to CP caused production of ROS, and it changes the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), Glutathione-S-transferase (GST) and malondialdehyde (MDA) in different tissues of experimental animals [13]. It is known that many antioxidant compounds and also antioxidant enzymes in biological systems prevent cell and tissue damages against oxidative stress [14]. It is well known that superoxide dismutase (SOD) catalase and glutathione peroxidase are the major endogenous antioxidant enzymes which play role in