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发育中神经系统的辐射损伤:神经元损伤机制

Irradiation injury to the developing nervous system: mechanisms of neuronal injury.

作者信息

Kameyama Y, Inouye M

机构信息

Department of Teratology and Genetics, Nagoya University, Japan.

出版信息

Neurotoxicology. 1994 Spring;15(1):75-80.

PMID:8090364
Abstract

Undifferentiated neural cells in the developing brain are particularly vulnerable to irradiation and easily involved in cell death. We investigated in mice cytological features of radiation-induced death of neuron-precursor cells and their high sensitivity. The acute cell injury in the embryonic telencephalon by doses as low as 0.1 Gy was not reversed up to 6 hours and injured cells expressed apoptotic death which began at 2 hours after exposure and peaked at 6-9 hours. Radiation-induced cell death in the cerebellar -external granular layer of newborn mice exposed to 0.24 Gy was suppressed completely by cycloheximide, a protein synthesis inhibitor. The high incidence of radiation-induced apoptosis of the telencephalic ventricular cells observed at the beginning of cortical neuron production could be attributed to the emergence of radiosensitive G1phase cells at this stage. One of the significant factors determining the period of high sensitivity for radiation-induced apoptosis could be a certain initial phase of chemical cytodifferentiation prior to their actual morphological differentiation.

摘要

发育中的大脑中未分化的神经细胞对辐射特别敏感,很容易发生细胞死亡。我们在小鼠中研究了辐射诱导的神经前体细胞死亡的细胞学特征及其高敏感性。胚胎端脑受到低至0.1 Gy剂量的急性细胞损伤在6小时内未得到逆转,受损细胞表现出凋亡性死亡,在暴露后2小时开始,在6 - 9小时达到峰值。用蛋白质合成抑制剂环己酰亚胺可完全抑制新生小鼠小脑外颗粒层暴露于0.24 Gy辐射后诱导的细胞死亡。在皮质神经元产生开始时观察到的端脑室细胞辐射诱导凋亡的高发生率可能归因于这个阶段出现的放射敏感G1期细胞。决定辐射诱导凋亡高敏感时期的一个重要因素可能是在实际形态分化之前化学细胞分化的某个初始阶段。

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