Contribution of Glutathione Peroxidase and Nitric Oxide to Potassium Bromate-Induced Oxidative Stress and Kidney Damage in Mice

Abstract

In order to confirm the participation of peroxynitrite in potassium bromate (KBrO₃)-induced oxidative stress and kidney damage in mice, we investigated effects of administration of nitric oxide (NO) synthase inhibitor on them. Cytoplasmic glutathione peroxidase (GPx) activity remarkably decreased within 3 hr after KBrO₃ administration, and then oxidative stress started to occur. However, kidney damage occurred 24 hr after KBrO₃ administration. Pre-administered N^G-monomethyl-L-arginine (L-NMMA), a NO synthase inhibitor, suppressed KBrO₃-induced oxidative stress and kidney damage. However, no effect of L-NMMA was observed on the KBrO₃-induced reduction of cytoplasmic GPx activity. These results suggest that reduction of cytoplasmic GPx activity resulted from the KBrO₃ administration initiates oxidative stress and that NO also participates in the promotion of KBrO₃-induced oxidative stress and kidney damage.