TBARS公司
化学
过氧化氢酶
谷胱甘肽
超氧化物歧化酶
过氧化氢
谷胱甘肽过氧化物酶
抗氧化剂
活性氧
谷胱甘肽还原酶
氧化应激
硫代巴比妥酸
内分泌学
生物化学
内科学
药理学
脂质过氧化
酶
生物
医学
作者
Hideaki Kabuto,Satoru Hasuike,Nobuko Minagawa,Tsuyoshi Shishibori
标识
DOI:10.1016/s0013-9351(03)00062-8
摘要
We investigated the modifications in endogenous antioxidant capacity, including superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, oxidative stress index, reduced glutathione (GSH), glutathione disulfide (GSSG), and thiobarbituric acid-reactive substance (TBARS) in the brain, liver, kidney, and testes of mice under bisphenol A (BPA), an endocrine disrupter, treated for 5 days. BPA was administrated intraperitoneally at doses of 25 and 50 mg/kg/day. The TBARS levels were not affected by BPA administrations. The SOD activities increased and the catalase activities decreased in the liver after BPA administration. The GPx activity decreased in the kidney. The levels of GSH+GSSG increased in the brain, kidney, liver, and testes, while, the levels of GSH decreased in the testes. SOD converts superoxide into hydrogen peroxide, and catalase and GPx convert hydrogen peroxide into hydrogen oxide. Our results suggest that the injection of BPA induces overproduction of hydrogen peroxide in the mouse organs. Hydrogen peroxide is easily converted to hydroxy radical. The decrease of GSH and the increase of GSSG may be caused by the hydroxy radical. BPA may show its toxicity by increasing hydrogen peroxide.
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