Vlassara Helen, Uribarri Jaime, Cai Weijing, Striker Gary
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA.
Ann N Y Acad Sci. 2008 Apr;1126:46-52. doi: 10.1196/annals.1433.055.
Increased oxidative stress (OS) underlies many chronic diseases prevalent in aging. Data in humans confirm the hypothesis that advanced glycation end products (AGEs) and other oxidants derived from the diet may be major contributors to increased OS in normal adults as well as those with diabetes mellitus or kidney failure. Mice fed a diet with a lowered (approximately 50%) content of AGEs or a typical calorie-restricted (CR) diet, accumulated a smaller amount of AGEs, maintained normal levels of AGE receptor-1 (AGER1), and did not have increased oxidant stress or cardiac or kidney fibrosis with aging. However, the findings in mice fed a CR diet with an increased content of AGEs resembled those in mice fed a nonrestricted diet that had the usual higher content of AGEs. Thus, there was an inverse correlation between the dietary AGE content, the AGER1 to receptor for AGE (RAGE) ratio, OS, organ damage, and life span. In both humans and mice, there was an inverse correlation between the AGER1 to RAGE ratio and the levels of OS.
氧化应激（OS）增加是衰老过程中许多常见慢性疾病的潜在原因。人体数据证实了这样一种假设，即饮食中产生的晚期糖基化终产物（AGEs）和其他氧化剂可能是导致正常成年人以及糖尿病或肾衰竭患者氧化应激增加的主要因素。喂食低（约50%）AGEs含量饮食或典型热量限制（CR）饮食的小鼠，AGEs积累量较少，AGE受体1（AGER1）维持正常水平，且不会随着衰老出现氧化应激增加或心脏或肾脏纤维化。然而，喂食AGEs含量增加的CR饮食的小鼠的研究结果与喂食正常高AGEs含量非限制饮食的小鼠相似。因此，饮食中AGE含量、AGER1与AGE受体（RAGE）的比例、氧化应激、器官损伤和寿命之间存在负相关。在人类和小鼠中，AGER1与RAGE的比例和氧化应激水平之间均存在负相关。
