Glycerol and Methylglyoxal Metabolism.
Glycerol and Methylglyoxal Metabolism.
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DOI：
10.1128/ecosalplus.3.4.3
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发表时间：
2005-11-01
期刊：
影响因子：
--
通讯作者：
Booth, Ian R
中科院分区：
文献类型：
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作者：
Booth, Ian R
甘油和丙酮醛（MG）之间的代谢联系主要是DHAP，它是甘油有氧分解的中间体，也是MG的主要前体，是丙酮醛合酶（MGS）的底物。MG的合成是不平衡代谢的结果，与磷酸盐限制或通过能够产生大量DHAP的途径的过量碳通量有关。产生MG的细胞产生毒素作为代谢失衡的生存的中间策略。事实上，在这一领域的代谢调节可以被视为一种策略，以避免死亡的自我中毒。甘油进入大肠杆菌和沙门氏菌血清型鼠伤寒是由水甘油孔蛋白，GlpF促进。鼠伤寒血清型中的同源蛋白PduF促进1，2-丙二醇（Ppd）进入，是Ppd代谢途径的一部分。MGS催化从DHAP中消除磷酸盐，形成从酶释放的酶结合的包合物（酸盐）中间体，然后释放无机磷酸盐。该酶对DHAP具有高度特异性。在E.大肠杆菌和血清型鼠伤寒杆菌，但占主导地位的途径是谷胱甘肽依赖性glycoproteinase III系统。KefB和KefC系统已经发展为在亲电体解毒期间提供保护。KefB和KefC是GSH门控的K+外排系统，通过解毒过程中产生的谷胱甘肽加合物的形成和结合来激活。
The metabolic connection between glycerol and methylglyoxal (MG) is principally that DHAP, which is an intermediate in the aerobic breakdown of glycerol, is also the major precursor of MG, being the substrate for methylglyoxal synthase (MGS). The synthesis of MG is a consequence of unbalanced metabolism related either to a limitation for phosphate or to excessive carbon flux through the pathways that have the capacity to generate significant pools of DHAP. Cells producing MG produce a poison as an intermediate strategy for survival of metabolic imbalance. Indeed the panoply of metabolic regulation in this sector of catabolism can be seen as a strategy to avoid death by self-poisoning. Glycerol entry into Escherichia coli and Salmonella enterica serovar Typhimurium is facilitated by the aquaglyceroporin, GlpF. A homologous protein in serovar Typhimurium, PduF, facilitates the entry of 1,2-propanediol (Ppd) and is part of the Ppd metabolic pathway. MGS catalyzes the elimination of phosphate from DHAP, forming an enzyme-bound enediol(ate) intermediate that is released from the enzyme, followed by release of inorganic phosphate. The enzyme is highly specific for DHAP. Multiple MG detoxification pathways are found in both E. coli and serovar Typhimurium, but the dominant pathway is the GSH-dependent glyoxalase III system. The KefB and KefC systems have evolved to provide protection during detoxification of electrophiles. KefB and KefC are GSH-gated K+ efflux systems that are activated by the formation and binding of glutathione adducts that are generated during detoxification.