Chronic UUO leads to progressive renal tubular atrophy and intersitital fibrosis that may be aggravated by production of reactive oxygen species(ROS). Obstructive nephropathy is frequently associated with chronic sodium wasting and consequent SD. Tissue damage by ROS is attenuated by AOE, including catalase (CAT), manganese superoxide dismutase (MnSOD), copper-zinc SOD (CuZnSOD), glutathione peroxidase (GPx) and glutathione-S-transferase(GST). To investigate the response of renal AOE to SD and UUO, adult male Sprague-Dawley rats were placed on normal sodium (NS)(16.22 mmol/kg/d) or SD(4.75 mmol/kg/d) diets and subjected to UUO or sham operation. Obstructed(UUO), intact opposite (IO), and sham kidneys were harvested after 4 d, the AOE activites measured in homogenates and expressed normalized to protein content. Results (mean± standard deviation, * designates p<0.05 vs NS, # designates p<0.05 vs Sham same Na): Table

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SD increased MnSOD, GPx and GST activities in Sham kidneys, and MnSOD and GPx in IO, but not in UUO. Relative to sham kidneys, UUO reduced renal CAT and GPx in both NS and SD and MnSOD in SD. These data show that SD increases AOE activity in normal kidney, perhaps indicative of a stress response to increased ROS in SD kidneys. UUO not only reduces AOE activity relative to Sham but also inhibited the increase due to SD. We conclude, therefore, that suppression of renal AOE by UUO may contribute to progression of renal injury in obstructive nephropathy. (Supported by NIH HL42057, DK44756 and DK45179).NIH Gm44263 and by NIH 5 P30 HD 27823