Role of peroxiredoxin-2 in protecting RBCs from hydrogen peroxide-induced oxidative stress.
Role of peroxiredoxin-2 in protecting RBCs from hydrogen peroxide-induced oxidative stress.
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DOI：
10.3109/10715762.2012.756138
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发表时间：
2013-03
影响因子：
3.3
通讯作者：
Rifkind JM
中科院分区：
文献类型：
--
作者：
Nagababu E;Mohanty JG;Friedman JS;Rifkind JM
通过比较来自PRDX 2敲除小鼠和超氧化物歧化酶-1（SOD 1）敲除小鼠和对照小鼠的血液，研究了过氧化物氧还蛋白-2（PRDX 2）在防止过氧化氢诱导的红细胞氧化应激中的作用。PRDX 2的缺失增加了高铁血红蛋白和血红素降解（氧化应激的标志物）的基础水平，并降低了红细胞的变形能力。在含氧量正常的条件下，在体外孵育，有和没有抑制过氧化氢酶，导致在一个滞后期，在此期间发生的血红素降解可以忽略不计，其次是一个更快的速率血红素降解的PRDX 2的情况下。PRDX 2敲除小鼠血红素降解的明显基础增加，以及体外孵育期间的滞后，意味着PRDX 2中和在细胞通过微循环时经历的短暂缺氧条件下体内产生的过氧化氢。
The role of peroxiredoxin-2 (PRDX2) in preventing hydrogen peroxide-induced oxidative stress in the red blood cell was investigated by comparing blood from PRDX2 knockout mice with superoxide dismutase-1 (SOD1) knockout and control mice. Loss of PRDX2 increased basal levels of methemoglobin and heme degradation (a marker for oxidative stress), and reduced red blood cell deformability. In vitro incubation under normoxic conditions, both with and without inhibition of catalase, resulted in a lag phase during which negligible heme degradation occurred followed by a more rapid rate of heme degradation in the absence of PRDX2. The appreciable basal increase in heme degradation for PRDX2 knockout mice, together with the lag during in vitro incubation, implies that PRDX2 neutralizes hydrogen peroxide generated in vivo under the transient hypoxic conditions experienced as the cells pass through the microcirculation.