锰离子对人红细胞中磷酸己糖途径的刺激作用：锰离子依赖性NADPH过氧化物酶活性的证据。

Stimulation of the hexose monophosphate pathway in the human erythrocyte by Mn2+: evidence for a Mn2+-dependent NADPH peroxidase activity.

作者信息

Bennun A, Needle M A, DeBari V A

出版信息

Biochem Med. 1985 Feb;33(1):17-21. doi: 10.1016/0006-2944(85)90121-8.

Abstract

In human RBC hemolysates, Mn2+ was found to stimulate the HMP as determined by the release of 14CO2 from [1-14C]glucose, providing activities of 125, 200, and 300% of basal at Mn2+ concentrations of 1, 10, and 100 mM, respectively. To explore the possibility that this stimulatory effect upon the HMP is a result of redox recycling of NADPH, RBC hemolysates were used to study NADPH oxidation. Mn2+, alone or in combination with a free radical-generating system, did not enhance the ability of hemolysates to oxidize NADPH. However, hemolysates + 10 mM H2O2 brought about a 10-fold increase in NADPH oxidation (0.51 +/- 0.05 nmole/min to 5.67 +/- 0.84 nmole/min) and the addition of 10 mM Mn2+ to this system increased the rate of oxidation to 34.10 +/- 2.97 nmole/min. Boiled hemolysates, either in the presence or absence of Mn2+, had some residual catalytic activity.

摘要

在人红细胞溶血产物中，发现Mn2+可刺激磷酸戊糖途径（HMP），这是通过[1-14C]葡萄糖释放14CO2来测定的，在Mn2+浓度分别为1、10和100 mM时，其活性分别为基础活性的125%、200%和300%。为了探究这种对磷酸戊糖途径的刺激作用是否是由于NADPH的氧化还原循环所致，利用红细胞溶血产物研究了NADPH的氧化。单独的Mn2+或与自由基生成系统联合使用时，均未增强溶血产物氧化NADPH的能力。然而，溶血产物+10 mM H2O2使NADPH氧化增加了10倍（从0.51±0.05纳摩尔/分钟增加到5.67±0.84纳摩尔/分钟），向该系统中添加10 mM Mn2+可使氧化速率提高到34.10±2.97纳摩尔/分钟。无论有无Mn2+存在，煮沸的溶血产物都有一些残余的催化活性。