Vol. 44, No. 6, May 1998 BIOCHEMISTRY and MOLECULAR BIOLOGY INTERNATIONAL Pages 1255-1263 EFFECT OF VITAMIN E ON ANTIOXIDANT ENZYMES AND NITRIC OXIDE IN ISCHEMIA- REPERFUSED KIDNEY INJURY Fevziye UYSAL*, Ferhan K.GiRGIN*, Sevgi TOZON*, Sevil ALDEMiR**, Eser YILDIRIM SOZMEN* *Ege University School of Medicine, Dept. of Biochemistry, Bornova, 35100, izmir-TURKEY ** Ege University School of Medicine, Dept. of Surgery, Bornova,35100, izmir-TURKEY Received December 19, 1997 Received after revision, January 28, 1998 SUMMARY The effects of Vitamin E administration on antioxidant enzyme activities and nitrite-nitrate levels of the reperfused rat kidney tissues were investigated by performing a 60 rain ischemia followed by 24 and 72 hours of reperfusion. Vitamin E administration or the placebo (SF) was applied as 100 mg/kg BW. As expected, catalase (CAT) (p<0.05) and superoxide dismutase (SOD) (p<0.05) activities of ischemia/reperfused (I/R) kidney tissue were lower and malondialdehyde (MDA) levels were higher than control kidneys in both SF and vitamin E treated groups following 24 h reperfusion. During reperfusion of long term (72 h), vitamin E triggered a decrease in the MDA levels in the ischemic tissue, while it did not provoke a significant effect on SOD and catalase activities. Total nitrite levels of ischemic tissues in both of the groups were higher than matched control kidneys and this elevation was more clear in the vitamin E treated group. Our results showed that vitamin E has a protective effect on I/R injury, by a direct chain breaking effect on lipid peroxidation (LPO) and hence preventing the nitric oxide (NO) reservoir of ischemic tissue. Alfa-tocopherol may be a promising agent for the prevention of tissue injury caused by free oxygen radicals. INTRODUCTION Oxygen derived radicals play a role in reperfusion injury (1-3) in various tissues including liver, heart, intestine and kidney as well as in the pathogenesis of some other diseases such as atherosclerosis, carcinogenesis, etc. They affect through inactivation of antioxidant enzymes, alterating the balance between oxidant-antioxidant status, hence leading to a variety of pathogenetic processes such as peroxidation of membrane lipids which cause cell damage. Under physiological conditions, cells contain endogenous protective agents with antioxidant properties, such as vitamin E, vitamin C or enzymatic scavengers such as SOD, catalase (CAT), Glutathione peroxidase (GSH-Px) (4). Nath et al demonstrated that dietary deficiency of vitamin E led to structural and functional renal impairment in rats at 24 hours after lh ischemia (5). It has also been shown that vitamin E has protective and therapeutic roles against the LPO observed after reperfusion both in animal models and in patients (6,7,8). To date, most studies have focused on the role of nitric oxide (NO) in ischemia-reperfusion (I/R) injury of heart and brain tissues (9). It has been shown that free radical mediated 1255 1039-9712/98/061255-09505.00/0 Copyright 9 1998 by Academic Press Australia. All rights of reproduction in any form reserved.