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 (KBrO 3)-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 KBrO 3 administration, and then oxidative stress started to occur. However, kidney damage occurred 24 hr after KBrO 3 administration. Pre-administered N G-monomethyl-L-arginine (L-NMMA), a NO synthase inhibitor, suppressed KBrO 3-induced oxidative stress and kidney damage. However, no effect of L-NMMA was observed on the KBrO 3-induced reduction of cytoplasmic GPx activity. These results suggest that reduction of cytoplasmic GPx activity resulted from the KBrO 3 administration initiates oxidative stress and that NO also participates in the promotion of KBrO 3-induced oxidative stress and kidney damage.