#5878 PROTECTIVE EFFECTS OF VITAMIN D ON HYPERANDROGENEMIA-INDUCED-ACUTE KIDNEY INJURY THROUGH THE INTERACTION WITH THE RAS/INOS PATHWAY

Abstract Background and Aims The onset development of metabolic abnormalities are closely related to polycystic ovary syndrome (PCOS). It has not yet been determined whether PCOS contributes kidney injury, the mechanism underlying condition is fully understood. Treatment with vitamin D shown have beneficial effects on women renal disease. This study investigated hypothesis that supplementation exerts renoprotective via regulating renin-angiotensin system (RAS)/inducible nitric oxide synthase (iNOS) pathway Method Female Sprague-Dawley rats were randomly divided into five groups (n = 10): (a) control, (b) sham, (c) dehydroepiandrosterone (DHEA, 6 mg/100 g day-1 S.Q.), (d) DHEA + (1000 IU/Kg; 3 days/week), (e) D. Plasma, ovary, levels angiotensin-converting enzyme (ACE) activity was using FAPGG-based colorimetric method. amount NO measured by determining concentrations nitrite nitrate end products in plasma tissue samples Griess Histopathological changes also evaluated. Results Plasma testosterone increased DHEA-treated compared controls, indicating a hyperandrogenic state. Further, hyperandrogenemia-induced-acute injury plasma, renal, ovarian activities association elevations urine levels; these reversed treatment. Conclusion Hyperandrogenemia causes systemic through RAS imbalance metabolism disturbances, followed apparent destruction tissues. Vitamin attenuated hyperandrogenemia-associated acute injuries, likely interaction RAS/iNOS pathway.