Dux E, Oschlies U, Uto A, Kusumoto M, Hossmann K A
Department of Experimental Neurology, Cologne, Germany.
Acta Neuropathol. 1996 Dec;92(6):541-4. doi: 10.1007/s004010050559.
Primary cortical and hippocampal neuronal cultures submitted to brief histotoxic hypoxia suffer delayed neuronal death after 24 h [Uto et al. (1995) J Neurochem 64: 2185-2192]. In this study the ultrastructural changes were monitored during the first 6 h following 5-min histotoxic hypoxia induced by exposure to 100 microM iodoacetate. In both cortical and hippocampal CA1 neurons, disaggregation of ribosomes was the earliest sign of histotoxic pathology. Vacuolizations of mitochondria, endoplasmic reticulum and Golgi apparatus, as well as fragmentation and disintegration of neurofilaments followed later. Signs of apoptotic nuclear degeneration were absent. Our observations demonstrate that, similar to that seen in ischemia, disaggregation of ribosomes after brief histotoxic hypoxia is one of the first pathological alterations heralding delayed neuronal death.
暴露于100微摩尔碘乙酸诱导的5分钟组织毒性缺氧后，原代皮质和海马神经元培养物在24小时后会出现延迟性神经元死亡[Uto等人（1995年）《神经化学杂志》64卷：2185 - 2192页]。在本研究中，对暴露于100微摩尔碘乙酸诱导的5分钟组织毒性缺氧后的最初6小时内的超微结构变化进行了监测。在皮质和海马CA1神经元中，核糖体解聚是组织毒性病理最早出现的迹象。线粒体、内质网和高尔基体的空泡化，以及神经丝的断裂和崩解随后出现。未观察到凋亡性核变性的迹象。我们的观察结果表明，与缺血时所见相似，短暂组织毒性缺氧后的核糖体解聚是预示延迟性神经元死亡的最早病理改变之一。
