[Frontiers in Bioscience, Elite, 7, 278-291, January 1, 2015] 278 1. ABSTRACT Cisplatin used in treatment of solid tumor induces oxidative stress which leads to hepatotoxicity and nephrotoxicity. New strategies are therefore needed to combat toxicity and optimize its therapeutic potential. Riboflavin (Vitamin B 2 ) under photoillumination works as an anti proliferative agent and induces apoptosis. These properties of riboflavin have been exploited to mitigate cisplatin induced toxicities. 9,10-dimethylbenz(a)anthracene /12-O-tetradecanoylphorbol-13-acetate were used to induce skin tumor in Swiss albino mice. The tumor induced mice were treated with cisplatin, riboflavin as well as their combination under photo illumination. In comparison to tumor control group the cisplatin and riboflavin treated groups showed a compromised level of antioxidant enzymes, functional markers and a higher degree of lipid peroxidation. However these parameters tended towards normal in the combination treated group. The results from histopathology indicate that apoptosis was favored mode of cell death and that necrosis was reduced in combination treated groups. Our findings indicate Riboflavin as adjuvant with cisplatin: Study in mouse skin cancer model Maria Salman 1 , Imrana Naseem 1 1 Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, U.P, India 202002 TABLE OF CONTENTS 1. Abstract 2. Introduction 3. Materials and methods 3.1. Materials 3.2. Animal husbandry and treatment 3.3. Preparation of samples 3.4. Histopathological processing 3.5. Biochemical estimations 3.6. Statistical analysis 4. Results 4.1. Effect of treatment on body weight and tumor volume 4.2. Effect of treatment on antioxidant enzymes 4.3. Effect on the levels of MDA and GSH 4.4. Effect of treatment on kidney and liver function markers in serum 4.5. Histopathology of mouse kidney, liver and skin 5. Discussion 6. Acknowledgements 7. References that combination of cisplatin with riboflavin under photo illumination synergizes its anti cancer activity towards cancer cells and attenuates the cisplatin induced toxicities. 2. INTRODUCTION Cisplatin (CP) is an effective anticancer chemotherapeutic drug widely used in the treatment of various malignant tumors including head and neck, ovarian, testicular, oesophageal and small cell lung cancer and many other solid tumors. It exerts its effect by the binding to DNA and non-DNA targets and then the induction of cell death through apoptosis, necrosis or both within the heterogeneous population of cells that forms a tumoral mass (1). It however elicits nephrotoxicity, hepatotoxicity, ototoxicity, gastrointestinal dysfunction and myelosuppression which are major setbacks in its clinical use (2). Although nephrotoxicity is considered as the dose limiting factor for CP use, hepatotoxicity can also occur at high doses (3). The