Spontaneous skin damage and delayed wound healing in SOD1-deficient mice
Spontaneous skin damage and delayed wound healing in SOD1-deficient mice
复制标题
DOI：
10.1007/s11010-010-0449-y
复制
发表时间：
2010-08-01
影响因子：
4.3
通讯作者：
Fujii, Junichi
中科院分区：
文献类型：
--
作者：
Iuchi, Yoshihito;Roy, Dipa;Fujii, Junichi
超氧化物歧化酶1(SOD1)是一种保护皮肤免受氧化应激的重要抗氧化酶。遗传背景为b129Sv小鼠的SOD1(-/-)小鼠在15周后出现面部皮肤损伤。眼睑肿胀为首发症状，并通过触发自我抓挠而造成损害。在20周的SOD1(-/-)小鼠中，背部伤口愈合所需的时间明显延迟。氧化应激标志物，4-羟基壬烯醛和硫代巴比妥酸反应物质，在创伤后第一天，SOD1(-/-)小鼠的水平出人意料地降低。静脉注射含氮自由基的电子顺磁共振信号强度衰减率表明，SOD(+/+)小鼠创面电子顺磁共振信号强度的半衰期明显延长。然而，尽管SOD1(-/-)小鼠对照皮肤的信号强度半衰期稍长一些，但损伤皮肤的信号强度半衰期没有改变。综上所述，这些数据表明SOD1(-/-)小鼠的皮肤处于氧化还原失衡状态，容易受到创伤的损害。
Superoxide dismutase 1 (SOD1) is an important antioxidative enzyme that protects skin from oxidative stress. SOD1 (-/-) mice with a genetic background of b129Sv mice showed facial skin damage after 15 weeks of age. Eyelid swelling occurred as the initial symptom and caused impairment by triggering self-scratching. The period required for wound healing in the back was markedly delayed in 20-week SOD1 (-/-) mice. Oxidative stress markers, 4-hydroxynonenal and thiobarbituric acid-reactive substances, were unexpectedly lower in SOD1 (-/-) mice at day 1 after wounding. The decay rate of electron paramagnetic resonance signal intensity of intravenously injected nitroxide radical indicated that the half-life of the signal intensity was significantly prolonged in the wounded skin of SOD1 (+/+) mice. However, while the half-life of the signal intensity in control skin was a little longer in SOD1 (-/-) mice, it did not change in wounded skin. Taken together, these data suggest that the skin of SOD1 (-/-) mice is in redox imbalance and prone to damage by wounding.