Increased liver-specific catalase activity in transgenic mice.

Increased liver-specific catalase activity in transgenic mice.
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转基因小鼠肝脏特异性过氧化氢酶活性增加。

DOI:
10.1089/dna.1996.15.625
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发表时间:
1996
影响因子:
3.1
通讯作者:
Spear,BT
Spear,BT
中科院分区:
生物学4区
文献类型:
--
作者:
Nilakantan,V;Li,Y;Glauert,HP;Spear,BT

文献摘要

被引文献

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过氧化氢酶是过氧化氢的主要解毒酶,被认为是维持细胞内低水平过氧化氢的关键。已有研究表明,过氧化物酶增殖物等外源物质引起的DNA氧化损伤和肿瘤发生可能与H_2O_2水平升高有关。为了开发一种小鼠模型系统来解决这个问题,我们培育了转基因小鼠,它们的肝脏过氧化氢酶水平增加了三到四倍。在转基因小鼠中,脂肪酰辅酶A(CoA)氧化酶和月桂酸羟基酶的活性没有变化,表明过氧化氢酶水平的升高不会改变这些由过氧化物体增殖物诱导的产生活性氧的酶的活性。这些小鼠应该有助于阐明过氧化氢在过氧化物体增殖物和其他外源物质介导的细胞事件中的作用。
Catatase is the major peroxisomal H2O2-detoxifying enzyme and is thought to be critical in maintaining low H2O2levels within a cell. It has been proposed that increased H2O2levels may be involved in oxidative DNA damage and tumor promotion induced by peroxisome proliferators and other xenobiotics. To develop a mouse model system to address this issue, we have generated transgenic mice that exhibit a three- to four-fold increase in liver catalase levels. The activities of fatty acyl coenzyme A (CoA) oxidase and lauric acid hydroxylase were unchanged in transgenic mice, demonstrating that elevated catalase levels did not alter the activity of these other peroxisome proliferator-induced enzymes that produce active oxygen. These mice should help elucidate the role of H2O2in cellular events mediated by peroxisome proliferators and other xenobiotics.