Potassium Bromate-lnduced Hyperuricemia Stimulates Acute Kidney Damage and Oxidative Stress

概要

論文の詳細を見る
Acute exposure of mice to potassium bromate (KBrO_3), which is a major disinfection by-product of ozonation and/or chlorination of bromide-containing raw waters, causes serious kidney failure and neuropathological disorders. We observed significant elevations of serum uric acid levels and xanthine oxidase activity by KBrO_3 administration (1.2 mmol/kg) with elevating relative kidney weight, serum creatinine levels and renal oxidative stress. Therefore, allopurinol was administered to KBrO_3-treated mice to examine if the elevation of blood uric acid levels causes acute kidney damage and renal oxidative stress. These KBrO_3-induced elevations were significantly prevented by intraperitoneal administration of allopurinol (10 or 50 mg/kg) and significant correlation between kidney damage and uric acid levels was observed. Reduction of catalase activity in the kidney of KBrO_3-treated mice, which results in the accumulation of hydrogen peroxide, was also restored by allopurinol. There were significant correlations between catalase activity and uric acid levels or kidney damage. Furthermore, in in vitro experiment, catalase activity was reduced in the presence of physiological concentration of uric acid (approximately 0.3 mM or more). These results suggest that the reduction of catalase activity by the elevation of blood uric acid levels is a major cause of KBrO_3-induced acute kidney damage. Allopurinol also suppressed KBrO_3-induced increases of renal thiobarbituric acid reactive substances levels and renal protein carbonyl levels of mice. Furthermore, significant correlation between oxidative stress and blood uric acid levels was observed. Therefore, KBrO_3 seems to cause hyperuricemic status which in turn brings about acute kidney damage and oxidative stress with reducing catalase activity.
公益社団法人日本薬学会の論文
2004-12-01

Potassium Bromate-lnduced Hyperuricemia Stimulates Acute Kidney Damage and Oxidative Stress

スポンサーリンク

概要

著者

関連論文

スポンサーリンク