Ischemic insult exacerbates acrolein-induced conduction loss and axonal membrane disruption in guinea pig spinal cord white matter
Ischemic insult exacerbates acrolein-induced conduction loss and axonal membrane disruption in guinea pig spinal cord white matter
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DOI：
10.1016/s0022-510x(03)00201-6
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发表时间：
2003-12-15
影响因子：
4.4
通讯作者：
Shi, RY
中科院分区：
文献类型：
--
作者：
Peasley, MA;Shi, RY
缺血损伤后细胞的破坏可能是由于继发性损伤机制，而不是氧-葡萄糖剥夺本身。我们研究了丙烯醛（脂质过氧化（LPO）和氧化应激的醛产物）对离体豚鼠脊髓缺血损伤后白色物质轴突的影响。我们已经发现，当单独应用时对脊髓无害的50 μ M丙烯醛在再灌注期间应用时，在暴露1至2小时后引起动作电位传导失败和膜破坏。缺血性损伤也加剧了200 μ M丙烯醛的作用。单独使用时会造成功能和解剖学损伤。与代谢中毒不同，丙烯醛介导的损伤不是轴突大小的函数，并且不影响双重和多重刺激的反应不应性。这些结果表明，脊髓轴突，除了经历升高的自由基，更容易受到丙烯醛攻击时，氧气和葡萄糖的水平低。我们的结论是，自由基和脂质过氧化反应一般，丙烯醛在特定的，可能在细胞破坏和功能丧失在这种损伤中发挥关键作用。(C)2003 Elsevier B. V.保留所有权利。
Cellular destruction following ischemic insult may be due to secondary injury mechanisms, not the oxygen-glucose deprivation itself We have examined the effect of acrolein, an aldehyde product of lipid peroxidation (LPO) and oxidative stress, on the axons in isolated guinea pig spinal cord white matter following ischemic insult. We have found that acrolein at 50 muM, which is unharmful to spinal cord when applied alone, causes action potential conduction failure and membrane disruption following I to 2 h of exposure when applied during the reperfusion period. Ischemic insult also exacerbates the effect of acrolein at 200 [M. which does inflict functional and anatomical damage when applied alone. Unlike metabolic poisoning, acrolein-mediated damage is not a function of axonal size and does not affect the refractoriness in response to dual and multiple stimuli. These results indicate that spinal cord axons, in addition to experiencing elevated free radicals, are more vulnerable to acrolein attack when the level of oxygen and glucose is low. We conclude that free radicals and lipid peroxidation in general, and acrolein in specific, may play a critical role in cellular destruction and functional loss in such injury. (C) 2003 Elsevier B.V. All rights reserved.