Potassium bromate (KBrO3) induces renal proliferative response and damage by elaborating oxidative stress

Many chemical compounds which induce oxidative stress in the tissue produce carcinogenesis either alone or act as a tumor promoter in carcinogen-initi ated animals after prolonged exposure. Here, we report that potassium broma te (KBrO3) induces renal proliferative response and damage by elaborating o xidative stress. KBrO3 administration dose dependently induced renal ornith ine decarboxylase (ODC) activity several fold compared to its activity in s aline-treated rats. Similarly renal DNA synthesis which has been measured a s [H-3]thymidine incorporation in DNA also increases. KBrO3 administration also depleted the level of renal glutathione and glutathione reductase acti vity in a time dependent manner. The maximum depletion in the levels of ren al glutathione and glutathione reductase activity was observed 3 h after KB rO3 treatment which was 60 and 40%, respectively, of saline-treated control s. Parallel to these changes, a sharp increase in the blood urea nitrogen a nd serum creatinine levels was observed which is indicative of the concurre nt renal damage. These results suggest that oxidant generating KBrO3 acts a s a potent proliferator of kidney and acts by producing oxidative damage. ( C) 1999 Elsevier Science Ireland Ltd. All rights reserved.