ORIGINAL PAPER Yılmaz Aksoy Æ Turgut Yapanoglu Æ Hu¨lya Aksoy A. Kadir Yildirim The effect of dehydroepiandrosterone on renal ischemia-reperfusion-induced oxidative stress in rabbits Received: 20 June 2003 / Accepted: 30 September 2003 / Published online: 31 October 2003 Ó Springer-Verlag 2003 Abstract Reactive oxygen species (ROS) can play an important role in the pathogenesis of ischemia-reper- fusion (I/R) injury. Dehydroepiandrosterone (DHEA) is one of the hormones secreted from adrenal glands, and in some studies it has been shown that DHEA has antioxidant properties. This experimental study was designed to determine the effect of DHEA on I/R-in- duced oxidative stress in rabbit kidney. Twenty-one rabbits were divided into three groups. Rabbits were subjected to 60 min of left renal pedicle occlusion followed by 24 h of reperfusion. DHEA (50 mg/kg) (I/R + DHEA group) or equal volume of vehicle (I/R group) was administered 3 h prior to ischemia. The control group received only laparotomy without I/R, DHEA or vehicle. At the end of the reperfusion peri- ods, rabbits were decapitated. Renal tissues were taken for determination of malondialdehyde (MDA) levels as an indicator of lipid peroxidation and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities as antioxidant enzymes. In the I/R group, while renal SOD and CAT activities were significantly lower, MDA levels were significantly higher than in the I/R + DHEA group and controls. In the I/R + DHEA group, enzyme activities and MDA levels were similar to the controls. There was no significant difference in terms of renal GPX activity among the groups. DHEA may have a beneficial effect on renal tissue against oxidative damage due to I/R by preventing decreases in some antioxidant enzyme activities. Keywords Renal ischemia-reperfusion Æ Dehydroepiandrosterone Æ Reactive oxygen species Æ Antioxidant enzymes Introduction Renal ischemia-reperfusion (I/R) injury could arise as a consequence of clinical conditions such as renal trans- plantation, shock, cardiac arrest, hemorrhage and renal artery surgery [1]. In clinical settings, evidence is emerging that reactive oxygen species (ROS) injury resulting from disorders in oxygen metabolism can play an important role in the pathophysiology of the kidney reperfusion injury following ischemia [2]. In body, formed ROS are eliminated by enzymatic and non- enzymatic antioxidants. But when free radicals are generated in excess or when the cellular antioxidant defense system is defective, they can stimulate chain reactions by interacting with proteins, lipids and nu- cleic acids, causing cellular dysfunction and even death. In such a situation, administration of antioxidants should therefore give potential benefit by neutralizing ROS [1, 2]. Dehydroepiandrosterone (DHEA) and de- hydroepiandrosterone sulphate (DHEAS) are the most abundant steroid hormones in the circulation. Al- though DHEA is known to have numerous biological and biochemical effects, and beneficial action on ath- erosclerosis, neuronal injury, diabetes, obesity, cancer, stress, and viral and bacterial infections [3, 4, 5], the mechanism underlying the protective effect of DHEA is not obvious. Several studies have investigated the effect of DHEA on the cellular antioxidant enzyme activities [6, 7] and DHEA administration is considered to prevent lipid peroxidation of cell membranes and make them more resistant to oxidative stress [5, 6, 7, 8]. In the present study, we aimed to investigate the effects of DHEA pretreatment on lipid peroxidation, superoxide dismutase (SOD), catalase (CAT) and Y. Aksoy (&) Æ T. Yapanoglu Department of Urology, Medical School, Atatu¨rk University, 25240 Erzurum, Turkey E-mail: yaksoy@yahoo.com Tel.: +90-442-3166333/2313-2334 Fax: +90-442-2354493 H. Aksoy Æ A. K. Yildirim Department Biochemistry, Medical School, Atatu¨rk University, Erzurum, Turkey Urol Res (2004) 32: 93–96 DOI 10.1007/s00240-003-0382-6