Aryl hydrocarbon receptor (AhR)-mediated induction of xanthine oxidase/xanthine dehydrogenase activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin
Aryl hydrocarbon receptor (AhR)-mediated induction of xanthine oxidase/xanthine dehydrogenase activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin
复制标题
DOI：
10.1006/bbrc.2001.4464
复制
发表时间：
2001-03-16
影响因子：
3.1
通讯作者：
Fujii-Kuriyama, Y
中科院分区：
文献类型：
--
作者：
Sugihara, K;Kitamura, S;Fujii-Kuriyama, Y
环境污染物 2,3,7,8-四氯二苯并-对二恶英 (TCDD) 会诱导小鼠肝脏中的黄嘌呤氧化酶和黄嘌呤脱氢酶 (XO/XDH) 活性，以及乙氧基试卤灵-O-脱烷基酶和甲氧基-试卤灵-O-脱烷基酶活性。当TCDD给小鼠单次口服剂量40μg/kg时，XO和XDH的活性在3天内增加了约三倍，并且增加的水平维持了4周。用5-甲基胆蒽治疗小鼠也诱导XO/XDH活性，但苯巴比妥和地塞米松没有效果。 TCDD 治疗后，小鼠肝脏中醛氧化酶（一种与 XO/XDH 相关的钼黄酶）的水平也提高了约 1.5 倍。在缺乏AhR基因的空白小鼠(AhR(-/-))中没有观察到TCDD和3-甲基胆蒽的诱导作用。 XO 和 XDH 活性由 TCDD 在杂合小鼠 (AhR(+/-)) 中诱导。 TCDD刺激肝脏中的脂质过氧化反应。 XO 和 XDH 的诱导产生活性氧，可能导致 TCDD 的各种毒性。 (C) 2001 年学术出版社。
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, induced xanthine oxidase and xanthine dehydrogenase (XO/XDH) activities, in addition to ethoxyresorufin-O-dealkylase and methoxy-resorufin-O-dealkylase activities in liver of mice. When TCDD was given to mice as a single oral dose of 40 mug/kg, the activities of XO and XDH increased about threefold within 3 days and the increased levels were maintained for 4 weeks. The treatment of mice with 5-methyl-cholanthrene also induced XO/XDH activities, but phenobarbital and dexamethasone had no effect. The level of aldehyde oxidase, a molybdenum flavoenzyme related to XO/XDH, in mouse liver was also enhanced about 1.5-fold by TCDD treatment. The inducing effect of TCDD and 3-methylcholanthrene was not observed in null mice (AhR(-/-)), which lack the AhR gene. XO and XDH activities were induced by TCDD in heterozygous mice (AhR(+/-)). The lipid peroxidation in liver was stimulated by TCDD. The induction of XO and XDH, which produces reactive oxygen species, may contribute to the various toxicities of TCDD. (C) 2001 Academic Press.