Aldehyde and Xanthine Oxidase Activities in Tissues of Streptozotocin-Induced Diabetic Rats: Effects of Vitamin E and Selenium Supplementation Tayyebeh Ghaffari & Mohammad Nouri & Amir Ata Saei & Mohammad-Reza Rashidi Received: 8 November 2011 / Accepted: 24 November 2011 / Published online: 10 January 2012 # Springer Science+Business Media, LLC 2012 Abstract Effects of vitamin E and selenium supplementation on aldehyde oxidase (AO) and xanthine oxidase (XO) activities and antioxidant status in liver, kidney, and heart of streptozo- tocin (STZ)-induced diabetic rats were examined. AO and XO activities increased significantly after induction of diabetes in rats. Following oral vitamin E (300 mg/kg) and sodium selenite (0.5 mg/kg) intake once a day for 4 weeks, XO activity de- creased significantly. AO activity decreased significantly in liver, but remained unchanged in kidney and heart of vitamin E- and selenium-treated rats compared to the diabetic rats. Total antioxidants status, paraoxonase-1 (PON1) and erythrocyte superoxide dismutase activities significantly decreased in the diabetic rats compared to the controls, while a higher fasting plasma glucose level was observed in the diabetic animals. The glutathione peroxidase activity remained statistically un- changed. Malondialdehyde and oxidized low-density lipopro- tein levels were higher in the diabetic animals; however, these values were significantly reduced following vitamin E and selenium supplementation. In summary, both AO and XO activities increase in STZ-induced diabetic rats, and vitamin E and selenium supplementation can reduce these activities. The results also indicate that administration of vitamin E and selenium has hypolipidemic, hypoglycemic, and antioxidative effects. It decreases tissue damages in diabetic rats, too. Keywords Streptozotocin-induced diabetes . Vitamin E . Selenium . Aldehyde oxidase . Xanthine oxidase . Paraxonase 1 Introduction Diabetes mellitus is the most significant chronic metabolic disease with the highest rate of prevalence and mortality worldwide. It is estimated that about 5% of the world population are affected by this metabolic disorder and the prevalence of adults with diabetes is estimated to increase by 122% from 135 million in 1995 to 300 million in 2025 [1]. According to a large body of evidence, reactive oxygen species (ROS) and oxidative stress may play a pivotal role in the development, pathogenesis, and complication of diabetes [2, 3]. However, the mechanism(s) of the oxidative stress and ROS formation in diabetes have not been fully understood [4]. There are several potential sources of ROS in diabetes such as auto-oxidative glycosylation, hyperketonemia, the induction of NAD(P)H oxidases, and xanthine oxidase activity [4–7]. Xanthine oxidase (EC 1.17.3.2, XO) is a cyto- solic molybdenum-containing enzyme that exists originally as dehydrogenase form; however, it could be converted to the oxidase form in some conditions either irreversibly by proteolysis or reversibly by sulfhydryl oxidation of the protein molecule. The reactions catalyzed by xanthine oxidase/dehydrogenase involve generation of two electrons. Xanthine dehydrogenase (XDH) utilizes NAD + as the electron acceptor, but XO uses molecular oxygen as an electron acceptor producing hydrogen peroxide and superoxide anion [8]. Therefore, XO can act as an important biological source of ROS, and the involvement of this enzyme in many T. Ghaffari : M. Nouri Biochemistry Department, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran T. Ghaffari Students’ Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran A. A. Saei : M.-R. Rashidi (*) Research Center for Pharmaceutical Nanotechnology, Tabriz University of Medical Sciences, Tabriz, Iran e-mail: rashidi@tbzmed.ac.ir Biol Trace Elem Res (2012) 147:217–225 DOI 10.1007/s12011-011-9291-7