Keelan J, Brand M P, Bates T E, Land J M, Clark J B, Heales S J
Department of Neurochemistry, Institute of Neurology, London, England.
Neurochem Res. 1996 Aug;21(8):923-7. doi: 10.1007/BF02532342.
Nitric oxide (NO.) has been implicated in the process of cerebral ischemia/reperfusion injury. We have examined the production of NO., as reflected by nitrite (NO2-) + nitrate (NO3-) accumulation, from synaptosomes isolated from neonatal or adult rat brain and subjected to a period of glucose and oxygen deprivation. There was a significant increase in the amount of NO2- + NO3- production from adult synaptosomes under these conditions, whereas there was no difference compared to control in the production of NO2- + NO3- from the neonatal synaptosomes. The total antioxidant status of the synaptosomes at these different stages of brain development was found to be the same. These data suggest that the vulnerability of the adult brain to ischemia/reperfusion injury may be associated with the production of NO. from nerve terminals. The ratios of antioxidant capacity to NO. production under such conditions have been shown here to be different between the neonatal and adult nerve terminals. Thus the well documented resistance of neonatal brain to ischemia/reperfusion injury may involve the neonatal nerve terminal being under less oxidative stress than the adult.
一氧化氮（NO.）与脑缺血/再灌注损伤过程有关。我们检测了从新生或成年大鼠脑部分离出的突触体在经历一段葡萄糖和氧气剥夺后，由亚硝酸盐（NO2-）+硝酸盐（NO3-）积累所反映的NO.生成情况。在这些条件下，成年突触体中NO2- + NO3-生成量显著增加，而新生突触体中NO2- + NO3-的生成与对照组相比没有差异。发现在脑发育的这些不同阶段突触体的总抗氧化状态是相同的。这些数据表明，成年脑对缺血/再灌注损伤的易感性可能与神经末梢产生NO.有关。在此已表明，在这种条件下，新生和成年神经末梢的抗氧化能力与NO.生成的比率是不同的。因此，新生脑对缺血/再灌注损伤有充分记录的抵抗力可能涉及新生神经末梢比成年神经末梢承受的氧化应激更小。
