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J.Health Sci., 47(6), 565-570, 2001
Contribution of Glutathione Peroxidase and Nitric Oxide to Potassium Bromate-Induced Oxidative Stress and Kidney Damage in Mice
Satoshi Watanabe,*, a Yoshihiro Yoshimura,b and Tetsuya Fukuia
aDepartment of Health Chemistry, bDepartment of Analytical Chemistry, Faculty of Pharmaceutical Sciences, Hoshi University 4-41, Ebara 2-chome, Shinagawa-ku, Tokyo 142-8501, Japan
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 NG-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.
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