It was of interest, therefore, to find out if there is any interaction between these two variables. Our results indicated that the body weight of exercised rats did not increase compared with that of sedentary control rats when both were given free access to food. Such exercise is considered of moderate intensity. In the present work we have confirmed an earlier observation that treatment with GA decreases body weight in rats, and also in humans. SE in control rats did not significantly affect the body weight, but it enhanced further the drop in body weights of adenine �C treated and GA �C treated healthy rats. The body growth depressive action of SE in our rats may be due to a lower intake of feed, although it has previously been reported that energy intake in the PK 44 phosphate hemodialysis patients of Koufaki et al was slightly but significantly increased. In this work, the adenine �C treated rats exhibited the urinary and plasma profile of several traditional and novel markers of renal damage, as reported by us and others. Most of these were improved in rats given either GA or SE, and even more so in rats given GA and subjected to SE at the same time, supporting our hypothesis that the ameliorative action of GA on adenine- induced CRF is further enhanced by SE. The use of novel urinary and plasma biomarkers has been recently highlighted as being able to detect subtle and early renal changes in both chronic and acute renal injury. In this work, both traditional and novel biomarkers measured in urine and plasma were nearly all in full agreement. Examples of these novel biomarkers used included 8-isoprostane, which is a prostaglandin -F2-like compound that belongs to the F2 isoprostane class. It is produced in vivo by the free radical-catalyzed peroxidation of arachidonic acid, and its concentration is increased in conditions and diseases involving PG 01 oxidative stress. Urinary 8-oxo-2��-deoxyguanosine concentration is another measure of oxidative DNA stress. Different modes of exercise, including SE, are established to be beneficial in CKD and its cardiovascular and other complications in humans and animals. The mechanism by which SE ameliorates CKD is not known with certainty, but it has been hypothesized that the basis of the obtained benefits are probably multifactorial, and include the beneficial effect of SE on the oxidative status of the tissues. Although there is no unanimity in the literature regarding the influence of exercise on inflammation and oxidative stress, moderate SE is believed to be effective in preventing inflammation and oxidative damage in tissues of rats, but severe/acute exercise has been shown to produce the opposite effect in humans and rats. In our present experiments employing moderate SE, we found that SE did not significantly alter the renal concentration/activity of the measured incidence of oxidative stress, probably reflecting the adequacy of the defensive antioxidant oxidative abilities in these animals.