溴酸钾诱导小鼠肾组织氧化应激研究

目的:探讨溴酸钾诱导小鼠肾组织氧化应激状态的改变,建立小鼠肾组织氧化应激模型。方法:200mg/kg溴酸钾腹腔注射诱导小鼠氧化应激,采用荧光酶标仪测定小鼠肾组织的抗氧化能力指数,HPLC测定小鼠血清中肌酐含量及肾组织中维生素C含量,分光光度法测定小鼠肾组织中丙二醛含量和谷胱甘肽过氧化物酶活力,Griess反应法测定血浆及肾组织的一氧化氮含量。结果:与正常组相比,腹腔注射溴酸钾后小鼠肾组织的抗氧化能力指数、维生素C及谷胱甘肽过氧化物酶水平均有不同程度下降,同时血清肌酐水平、肾组织中丙二醛含量、血浆及肾组织中一氧化氮水平也不同程度升高。结论:溴酸钾诱导的氧化应激可导致肾组织损伤,其机制可能与肾组织的内源性抗氧化能力降低及氧自由基产生过多和蓄积有关。

Studies of potassium bromate-induced oxidative stress in murine kidneys

Objective: To investigate the changes of potassium bromate (KBrO3)-induced oxidative stress in kidneys of mice. Methods: In the time-course experiments on the oxidative stress status caused by KBrO3, mice received a single ip administration of KBrO3 dissolved in 0.9% NaCl at a dose of 200mg/kg. Oxygen radical absorbance capacity (ORAC) in kidneys was determined by automated multifunctional microplate reader. Serum creatinine level and the contents of Vitamin C in kidneys were determined by HPLC. Spectrophotometric method was performed to detect the levels of malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activity in kidneys. Griess method was performed to detect NO levels in plasma and kidneys. Results: Compared with the normal group, ORAC activity and the contents of Vitamin C and GSH-Px in kidneys decreased in mice treated with KBrO3. In contrast, serum creatinine level and the contents of MDA in kidneys and NO levels in plasma and kidneys increased in the same schedule. Conclusion: KBrO3-induced oxidative stress can result in kidney damage, which may be related to the decrease of scavenging activity in free radical and the increase of oxygen radicals in murine kidneys.