Molecular Dynamics Section, National Institute on Aging, National Institutes of Health , Baltimore, MD 21224, USA.
Free Radic Res. 2013 Mar;47(3):164-71. doi: 10.3109/10715762.2012.756138. Epub 2013 Jan 9.
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.
研究人员通过比较 PRDX2 基因敲除小鼠、SOD1 基因敲除小鼠和对照组小鼠的血液,探究了过氧化物酶 2(PRDX2)在防止红细胞内过氧化氢引起的氧化应激中的作用。PRDX2 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。在常氧条件下进行体外孵育,无论是否抑制过氧化氢酶,都会导致一个潜伏期,在此期间几乎没有血红素降解,而在没有 PRDX2 的情况下,血红素降解的速度会更快。PRDX2 基因敲除小鼠血红素降解的显著基础增加,以及体外孵育过程中的潜伏期,意味着 PRDX2 可以中和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。