可逆性脑缺血多胺代谢。

W Paschen
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引用次数: 0

摘要

腐胺、亚精胺和精胺的合成受关键酶鸟氨酸脱羧酶(ODC)和s -腺苷蛋氨酸脱羧酶(SAMDC)活性的控制。除了在细胞生长过程中的功能外,多胺,特别是腐胺在细胞膜钙相关事件中发挥作用,将细胞外刺激与细胞内反应(第二信使样反应)耦合,调节线粒体(精胺)的钙缓冲能力,并且,如果存在于细胞外腔室,调节n -甲基- d -天冬氨酸受体(亚精胺和精胺)的活性。可逆性脑缺血引发多胺代谢的病理紊乱,其特征是ODC合成急剧增加,即使在最脆弱的海马CA1亚区,也会同时出现总体蛋白合成严重抑制,SAMDC合成的明显抑制与总体蛋白合成的抑制并行。ODC免疫组化显示,观察到的变化是神经元对可逆性缺血的反应。这些酶活性的变化导致ODC活性的产物腐胺的形成过量。长时间再循环后,易受伤害的大脑结构中的精胺水平显著降低。此外,越来越多的证据表明,多胺可能在缺血期间和长时间的再循环后从细胞中释放出来,此时细胞明显坏死。本文将总结缺血诱导的多胺代谢紊乱的主要特征以及对相关细胞可能产生的后果,同时考虑到潜在的变化可能表明神经元从可逆缺血产生的代谢应激中恢复过程的激活或导致神经元坏死表现的病理性紊乱。阐明多胺代谢的化学后紊乱机制,有助于更好地理解不同病理刺激后神经元坏死发生的分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Polyamine metabolism in reversible cerebral ischemia.

Synthesis of the polyamines putrescine, spermidine, and spermine is controlled by the activity of the key enzymes ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC). Beside their function in cellular growth processes, polyamines and particularly putrescine play a role in calcium-related events at the cell membrane, coupling an extracellular stimulus to an intracellular response (second messenger-like reactions), modulate the calcium-buffering capacity of mitochondria (spermine), and, if present in the extracellular compartment, modulate the activity of the N-methyl-D-aspartate receptor (spermidine and spermine). Reversible cerebral ischemia triggers pathological disturbances in polyamine metabolism that are characterized by a sharp increase in ODC synthesis, even in the most vulnerable hippocampal CA1 subfield in which overall protein synthesis is severely depressed at the same time, and a marked suppression of SAMDC synthesis in parallel with the inhibition of overall protein synthesis. ODC immunohistochemistry has revealed that the observed changes are neuronal responses to reversible ischemia. These changes in enzyme activities result in an overshoot in the formation of putrescine, the product of ODC activity. Spermine levels are significantly reduced in vulnerable brain structures after prolonged recirculation. In addition, evidence is accumulating that polyamines may be released from the cell during ischemia and after prolonged recirculation at a time when cell necrosis is apparent. This review will summarize the major features of ischemia-induced disturbances in polyamine metabolism and the possible consequences for the cells involved, taking into account that the underlying changes may be indicative of either the activation of a recovery process of neurons from the metabolic stress produced by reversible ischemia or pathological disturbances resulting in the manifestation of neuronal necrosis. Elucidating the mechanisms responsible for the postischemic disturbances in polyamine metabolism may lead to a better understanding of the molecular mechanisms involved in the development of neuronal necrosis after different pathological stimuli.

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