• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Archives of microbiology >Methylglyoxal production in bacteria: suicide or survival? [Review]
【24h】

Methylglyoxal production in bacteria: suicide or survival? [Review]

机译：细菌产生的甲基乙二醛：自杀还是生存？ [评论]

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Methylglyoxal is a toxic electrophile. In Escherichia coli cells, the principal route of methylglyoxal production is from dihydroxyacetone phosphate by the action of methylglyoxal synthase. The toxicity of methylglyoxal is believed to be due to its ability to interact with the nucleophilic centres of macromolecules such as DNA. Bacteria possess an array of detoxification pathways for methylglyoxal. In E. coli, glutathione-based detoxification is central to survival of exposure to methylglyoxal. The glutathione-dependent glyoxalase I-II pathway is the primary route of methylglyoxal detoxification, and the glutathione conjugates formed can activate the KefB and KefC potassium channels. The activation of these channels leads to a lowering of the intracellular pH of the bacterial cell, which protects against the toxic effects of electrophiles. In addition to the KefB and KefC systems, E. coli cells are equipped with a number of independent protective mechanisms whose purpose appears to be directed at ensuring the integrity of the DNA. A model of how these protective mechanisms function will be presented. The production of methylglyoxal by cells is a paradox that can be resolved by assigning an important role in adaptation to conditions of nutrient imbalance. Analysis of a methylglyoxal synthase-deficient mutant provides evidence that methylglyoxal production is required to allow growth under certain environmental conditions. The production of methylglyoxal may represent a high-risk strategy that facilitates adaptation, but which on failure leads to cell death. New strategies for antibacterial therapy may be based on undermining the detoxification and defence mechanisms coupled with deregulation of methylglyoxal synthesis. [References: 51]
机译：甲基乙二醛是有毒的亲电子试剂。在大肠杆菌细胞中，甲基乙二醛生产的主要途径是通过甲基乙二醛合酶的作用从磷酸二羟基丙酮产生的。甲基乙二醛的毒性被认为是由于其与大分子如DNA的亲核中心相互作用的能力。细菌具有一系列甲基乙二醛的解毒途径。在大肠杆菌中，基于谷胱甘肽的排毒对于暴露于甲基乙二醛的存活至关重要。谷胱甘肽依赖性乙二醛酶I-II途径是甲基乙二醛解毒的主要途径，形成的谷胱甘肽共轭物可以激活KefB和KefC钾通道。这些通道的激活导致细菌细胞的细胞内pH降低，从而防止了亲电试剂的毒性作用。除了KefB和KefC系统外，大肠杆菌细胞还配备了许多独立的保护机制，其目的似乎旨在确保DNA的完整性。将介绍这些保护机制如何发挥作用的模型。细胞产生甲基乙二醛是一个悖论，可以通过在适应营养失衡状况中发挥重要作用来解决。对甲基乙二醛合酶缺陷型突变体的分析提供了证据，证明甲基乙二醛的生产需要允许在某些环境条件下生长。甲基乙二醛的产生可能代表了促进适应的高风险策略，但失败会导致细胞死亡。抗菌治疗的新策略可能是基于破坏解毒和防御机制以及甲基乙二醛合成的失控。 [参考：51]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号