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产生活性氧的神经毒性氨基酸所导致的细胞损伤的分子机制。

Molecular mechanisms of cellular injury produced by neurotoxic amino acids that generate reactive oxygen species.

作者信息

Metodiewa D

机构信息

Institute of Applied Radiation Chemistry, Technical University of Lódź, Poland.

出版信息

Amino Acids. 1998;14(1-3):181-7. doi: 10.1007/BF01345260.

DOI:10.1007/BF01345260
PMID:9871459
Abstract

There is now strong experimental evidence that the basic precursors for the synthesis of catechol(amine) and indolamine neurotransmitters, tyrosine and tryptophan can act as generators of ROS (reactive oxygen species): peroxides, superoxide and peroxyradicals. The consequences of free radicals formation from precursors during oxidative degradation process, their possible participation in electron transfer/addition reactions and chain processes involving cell antioxidant defense system were presented and discussed. Although the generation of neurotoxic ROS by tyrosine and tryptophan is accepted to occur in the presented model systems, doubts can exist as to the situation in vivo, which may be completely different and remain to be explored. The relevance of the present findings with regard to a variety of neurological diseases cannot be ignored.

摘要

现在有强有力的实验证据表明,儿茶酚(胺)和吲哚胺神经递质合成的基本前体——酪氨酸和色氨酸可作为活性氧(ROS)的生成剂:过氧化物、超氧化物和过氧自由基。本文介绍并讨论了氧化降解过程中前体形成自由基的后果、它们可能参与的电子转移/加成反应以及涉及细胞抗氧化防御系统的链式反应。虽然在本文所呈现的模型系统中,酪氨酸和色氨酸会生成具有神经毒性的ROS这一点已被认可,但对于体内情况仍可能存在疑问,因为体内情况可能完全不同,有待进一步探索。当前研究结果与多种神经系统疾病的相关性不容忽视。

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