Regulative potential of glutamine - Relation to glutathione metabolism
Regulative potential of glutamine - Relation to glutathione metabolism
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DOI：
10.1016/s0899-9007(01)00797-3
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发表时间：
2002-03-01
期刊：
影响因子：
4.4
通讯作者：
Spittler, A
中科院分区：
文献类型：
--
作者：
Roth, E;Oehler, R;Spittler, A
谷氨酰胺（GLN）是人体内最丰富的游离氨基酸（AA）。在细胞体外培养时获得的无GLN条件下，组织细胞不能生长。因此，当将GLN归类为“非必需”AA时，必须考虑到人体内GLN是由必需AA合成的，并不断地从骨骼肌输送到其他器官。令人着迷的是，像 GLN 这样相对简单的 AA 可以刺激多种细胞反应。 GLN不仅刺激细胞生长，还刺激表面抗原的表达、细胞因子的形成和热休克蛋白的合成。此外，GLN缺乏导致细胞周期停滞在Go至G，并减少细胞凋亡。有趣的是，许多这些生物活性也与细胞的还原氧势有关，这主要取决于还原型谷胱甘肽与氧化型谷胱甘肽的比率。实验动物研究表明，给予 GLN 可以增加还原型谷胱甘肽的组织浓度。本综述描述了 GLN 与还原型谷胱甘肽代谢的关系，并讨论了还原型谷胱甘肽代谢在各种临床条件下的变化，如再灌注损伤、心肌梗死、呼吸功能不全、癌症、糖尿病、肝病和临床蛋白质分解代谢。 (C) 爱思唯尔科学公司。2002 年。
Glutamine (GLN) is the most abundant free amino acid (AA) in the human body. Under GLN-free conditions, which can be obtained when cells are cultivated in vitro, tissue cells cannot grow. Therefore, when classifying GLN as a "non-essential" AA, one must consider that in the human body GLN is synthesized from essential AAs and is continuously delivered from skeletal muscle to other organs. It is fascinating that a relatively simple AA like GLN can stimulate a large variety of cellular reactions. GLN stimulates not only the growth of cells but also the expression of surface antigens, the formation of cytokines, and the synthesis of heat shock proteins, Further, a GLN deficiency leads to a cell cycle arrest in Go to G, and reduces apoptosis. Interestingly, many of these biological activities also are associated with the cellular reduced oxygen potential, which depends mainly on the ratio of reduced to oxidized Glutathione. Experimental animal studies have shown that the administration of GLN increases tissue concentrations of reduced glutathione. This review describes the relation of GLN to reduced glutathione metabolism and discusses the alteration of reduced glutathione metabolism under a variety of clinical conditions such as reperfusion injury, myocardial infarction, respiratory insufficiency, cancer, diabetes, liver disease, and clinical protein catabolism. (C) Elsevier Science Inc. 2002.