24 Protective effect of ethanolic extract of Grewia carpinifolia leaves on vanadium induced toxicity Olamide E. Adebiyi 1* , Ayobami D. Obisesan 1 , Funsho O. Olayemi 1 , James O. Olopade 2 1 Department of Veterinary Physiology, Biochemistry and Pharmacology, 2 Department of Veterinary Anatomy, University of Ibadan ABSTRACT: Key Words: vanadium, Grewia carpinifolia, haematology, serum biochemistry, Swiss mice Pentavalent vanadium (metavanadate salt) toxicity is a challenging environmental hazard that affects living organisms. Studies have shown that plants play important roles in protecting against heavy metal toxicity. This study was designed to evaluate the protective activity of ethanolic extracts of Grewia carpinifolia leaves following vanadium toxicity. Twenty-five male Swiss mice were randomly divided into five groups (A–E) of five rats each. Group A rats served as control and were given distilled water, Group B was administered with sodium metavanadate and a known antioxidant agent; α-tocopherol, Groups C and D were administered with sodium metavanadate and ethanolic extract of Grewiacarpinifolia leaves orally at 100 and 200 mg/kg body weight respectively while Group E was administered with only sodium metavanadate. After a daily single oral dosing for seven days, changes in behaviour, haematology and serum biochemistry parameters were analysed. Sodium metavanadate caused a significant decrease (p≤0.05) in haematocrit levels, haemoglobin (Hb) concentration, white blood cell count, neutrophil count and serum cholesterol level. A significant (p≤0.05) lymphocytosis was also observed in the group administered with sodium metavanadate alone. G.carpinifolia extract given concomitantly with sodium metavanadate was able to restore PCV, Hb concentrations and serum total protein to levels comparable with the control and standard groups. Grewia carpinifolia also significantly reduced the elevated serum levels of AST and ALT after vanadium induced hepatotoxicity. Our findings suggest that G. carpinifolia extract protected against the toxicity induced by vanadium; the plant extract at 200 mg/kg however appear to offer a better protection. Corresponding author: Adebiyi Olamide Elizabeth; olamideadebiyiade2015@yahoo.com 1. INTRODUCTION Vanadium is a heavy transition metal (Habib and Ibrahim, 2011), which has been recognized to be acutely toxic by most routes of introduction following environmental exposure in large doses. Disposition of vanadium in specific tissues may be involved in the pathogenesis of certain neurological disorders and cardiovascular diseases (Venkataraman and Sudha, 2005). Human activities such as combustion of fossil fuels (Aragón and Altamirano-Lozano, 2001), inhalation in the vicinity of metallurgical plants in addition to oil exploratory activities as seen in the Niger Delta region of Nigeria have further led to environment exposure to vanadium. Consequently, this has impacted negatively on the aquatic and terrestrial habitats in this region which represents about 12% of Nigeria's total surface area with over 28 million inhabitants (Federal Government of Nigeria, 1991). Vanadium compounds are acutely toxic by most routes of introduction following environmental exposure in most species. In general, the toxicity of vanadium compounds is linked to its oxidation state or valency, which increases with the oxidation state (Erdmann et al. 1984; Venkataraman and Sudha, 2005) Vanadium within the cells has predominantly an oxidation state of +4 as a result of reactions with intracellular antioxidants (Aureliano and Gândara, 2005; Kordowiak and Holko, 2009). Furthermore, vanadium compounds in the +4 oxidation state are oxidized by atmospheric oxygen to the +5 oxidation state with accompanying emission of a superoxide anion radical and generation of a hydroxyl radical via a Fenton-like reaction (Cuesta et al., 2011). Following Alexandria Journal of Veterinary Sciences 2015, 47: 1-6 ISSN 1110-2047, www.alexjvs.com DOI: 10.5455/ajvs.189645