Stoppa Graziela R, Cesquini Maristela, Roman Erika A F R, Ogo Satie H, Torsoni Marcio A
Departamento de Bioquímica-Instituto de Biologia-Universidade de Campinas-SP-Brazil.
Life Sci. 2006 Feb 16;78(12):1352-61. doi: 10.1016/j.lfs.2005.07.031. Epub 2005 Oct 17.
Non-enzymatic glycation is implicated in the development of various diseases such as Alzheimer's and diabetes mellitus. However, it is also observed during the physiologic process of aging. There is considerable interest in the contribution of oxidative stress to diabetes mellitus. An increase in the generation of reactive oxygen species can occur by non-enzymatic glycation and glucose autoxidation. Both of these processes lead to the formation of AGEs (Advanced glycation end-products) that contribute to the irreversible modification of enzymes, proteins, lipids and DNA. In this study, the effect of chronic hyperglycemia on the antioxidant system of diabetic rats was evaluated. The working hypothesis is that the loss of glucose homeostasis reduces the capacity to respond to oxidative damage. The enzymatic activities of CAT (catalase), GPx (gluthatione peroxidase), GR (gluthatione reductase) and GSH (reduced gluthatione) were increased in the blood of healthy rats subjected to endurance training, whereas, in diabetic rats the activities of CAT, GPx and GR were unaltered by similar training. SOD showed low activity in endurance-trained rats. The administration of aminoguanidine (an inhibitor of glycation reactions) in the drinking water increased the activities of CAT, GPx and GR, suggesting that glycation may be responsible for the partial inactivation of these enzymes. These results indicate that the association of hyperglycemia with strenuous physical exercise may induce cellular damage by impairing the antioxidant defense system.
非酶糖基化与多种疾病的发生发展有关，如阿尔茨海默病和糖尿病。然而，在衰老的生理过程中也会观察到这种现象。氧化应激对糖尿病的影响备受关注。非酶糖基化和葡萄糖自氧化可导致活性氧生成增加。这两个过程都会导致晚期糖基化终产物（AGEs）的形成，AGEs会对酶、蛋白质、脂质和DNA造成不可逆的修饰。在本研究中，评估了慢性高血糖对糖尿病大鼠抗氧化系统的影响。研究的假设是葡萄糖稳态的丧失会降低对氧化损伤的反应能力。耐力训练的健康大鼠血液中过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）的酶活性以及还原型谷胱甘肽（GSH）水平升高，而在糖尿病大鼠中，类似训练对CAT、GPx和GR的活性没有影响。超氧化物歧化酶（SOD）在耐力训练大鼠中的活性较低。饮用水中添加氨基胍（一种糖基化反应抑制剂）可提高CAT、GPx和GR的活性，这表明糖基化可能是这些酶部分失活的原因。这些结果表明，高血糖与剧烈体育锻炼相结合可能会通过损害抗氧化防御系统而导致细胞损伤。
