Molecular and Computational Biology Section, Ray R. Irani Hall-RRI 201, University of Southern California, Los Angeles, CA 90089-2910, USA.
Appl Environ Microbiol. 2010 Dec;76(24):7925-30. doi: 10.1128/AEM.01369-10. Epub 2010 Oct 15.
Glycation, or nonenzymatic glycosylation, is a chemical reaction between reactive carbonyl-containing compounds and biomolecules containing free amino groups. Carbonyl-containing compounds include reducing sugars such as glucose or fructose, carbohydrate-derived compounds such as methylglyoxal and glyoxal, and nonsugars such as polyunsaturated fatty acids. The latter group includes molecules such as proteins, DNA, and amino lipids. Glycation-induced damage to these biomolecules has been shown to be a contributing factor in human disorders such as Alzheimer's disease, atherosclerosis, and cataracts and in diabetic complications. Glycation also affects Escherichia coli under standard laboratory conditions, leading to a decline in bacterial population density and long-term survival. Here we have shown that as E. coli aged in batch culture, the amount of carboxymethyl lysine, an advanced glycation end product, accumulated over time and that this accumulation was affected by the addition of glucose to the culture medium. The addition of excess glucose or methylglyoxal to the culture medium resulted in a dose-dependent loss of cell viability. We have also demonstrated that glyoxylase enzyme GloA plays a role in cell survival during glycation stress. In addition, we have provided evidence that carnosine, folic acid, and aminoguanidine inhibit glycation in prokaryotes. These agents may also prove to be beneficial to eukaryotes since the chemical processes of glycation are similar in these two domains of life.
糖基化，或非酶糖基化，是一种含有活性羰基化合物与含有游离氨基基团的生物分子之间的化学反应。含羰基化合物包括还原糖如葡萄糖或果糖、碳水化合物衍生的化合物如甲基乙二醛和乙二醛、以及非糖如多不饱和脂肪酸。后一组包括蛋白质、DNA 和氨基酸脂等分子。已证明糖基化诱导的这些生物分子损伤是人类疾病如阿尔茨海默病、动脉粥样硬化和白内障以及糖尿病并发症的一个促成因素。糖基化也会影响标准实验室条件下的大肠杆菌，导致细菌种群密度下降和长期存活。在这里，我们已经表明，随着大肠杆菌在分批培养中老化，羧甲基赖氨酸（一种晚期糖基化终产物）的量随时间积累，并且这种积累受到培养基中葡萄糖添加的影响。向培养基中添加过量的葡萄糖或甲基乙二醛会导致细胞活力呈剂量依赖性丧失。我们还证明了糖基化酶 GloA 在糖基化应激期间对细胞存活起作用。此外，我们提供了证据表明肌肽、叶酸和氨基胍抑制原核生物中的糖基化。由于糖基化的化学过程在这两个生命领域中相似，这些试剂也可能对真核生物有益。
