Overexpression of Cu21/Zn21 Superoxide Dismutase Protects Against Early Diabetic Glomerular Injury in Transgenic Mice

Ex vivo and in vitro observations implicate superoxide as a mediator of cell injury in diabetes, but in vivo evi-dence is lacking. In the current studies, parameters of glomerular injury were examined in hemizygous non-diabetic transgenic mice (SOD) and streptozotocin-diabetic (D) transgenic mice (D-SOD), which overex-press human cytoplasmic Cu21/Zn21 superoxide dis-mutase (SOD-1), and in corresponding wild-type littermates (WT, D-WT) after 4 months of diabetes. In both SOD and D-SOD mice, renal cortical SOD-1 activity was twofold higher than values in the WT mice; blood glucose and glycosylated hemoglobin (GHb) levels did not differ in the two diabetic groups. Urinary albumin excretion, fractional albumin clearance, urinary transforming growth factor-b (TGF-b) excretion, glo