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低压缺氧诱导小鼠肝脏乙二醛酶I

Induction of mouse liver glyoxalase I by hypobaric hypoxia.

作者信息

Principato G B, Talesa V, Norton S J, Contenti S, Mangiabene C, Rosi G

机构信息

Department of Experimental Medicine, University of Perugia, Italy.

出版信息

Biochem Int. 1990;20(6):1019-23.

PMID:2369408
Abstract

Hypobaric hypoxia at 0.45 atm induced a reversible increase of mouse liver glyoxalase I. The levels of this enzyme increased after an exposure of 20 h and 20 + 20 h, whereas the activity decreased to the control values after 20 h at room pressure. Before the treatment, some animals received tritiated leucine (i.p.). Glyoxalase I was purified to homogeneity. The pure enzyme from the treated animals showed 20-times more radioactivity than the controls. Thus, the increase in specific activity is due to new protein synthesized in response to the treatment at 0.45 atm. The activities of glyoxalase II and glutathione S-transferase were not affected by the treatment.

摘要

0.45个大气压下的低压缺氧诱导小鼠肝脏乙二醛酶I可逆性增加。暴露20小时和20 + 20小时后,该酶水平升高,而在室温常压下暴露20小时后活性降至对照值。在处理前,一些动物腹腔注射了氚标记的亮氨酸。乙二醛酶I被纯化至同质。来自处理动物的纯酶显示出比对照高20倍的放射性。因此,比活性的增加是由于在0.45个大气压处理后合成的新蛋白质所致。乙二醛酶II和谷胱甘肽S -转移酶的活性不受该处理的影响。

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