Edeas M, Attaf D, Mailfert A-S, Nasu M, Joubet R
Société française des antioxydants, International Antioxidants Task Force, 15, rue de la Paix, 75002 Paris, France.
Pathol Biol (Paris). 2010 Jun;58(3):220-5. doi: 10.1016/j.patbio.2009.09.011. Epub 2009 Dec 23.
Glycation and oxidative stress are two important processes known to play a key role in complications of many disease processes. Oxidative stress, either via increasing reactive oxygen species (ROS), or by depleting the antioxidants may modulate the genesis of early glycated proteins in vivo. Maillard Reactions, occur in vivo as well as in vitro and are associated with the chronic complications of diabetes, aging and age-related diseases. Hyperglycaemia causes the autoxidation of glucose, glycation of proteins, and the activation of polyol metabolism. These changes facilitate the generation of reactive oxygen species and decrease the activity of antioxidant enzymes such as Cu,Zn-superoxide dismutase, resulting in a remarkable increase of oxidative stress. A large body of evidence indicates that mitochondria alteration is involved and plays a central role in various oxidative stress-related diseases. The damaged mitochondria produce more ROS (increase oxidative stress) and less ATP (cellular energy) than normal mitochondria. As they are damaged, they cannot burn or use glucose or lipid and cannot provide cell with ATP. Further, glucose, amino acids and lipid will not be correctly used and will accumulate outside the mitochondria; they will undergo more glycation (as observed in diabetes, obesity, HIV infection and lipodystrophia). The objective of this paper is to discuss how to stop the vicious circle established between oxidative stress, Maillard Reaction and mitochondria. The potential application of some antioxidants to reduce glycation phenomenon and to increase the antioxidant defence system by targeting mitochondria will be discussed. Food and pharmaceutical companies share the same challenge, they must act now, urgently and energetically.
糖基化和氧化应激是已知在许多疾病过程的并发症中起关键作用的两个重要过程。氧化应激，要么通过增加活性氧（ROS），要么通过消耗抗氧化剂，可能在体内调节早期糖化蛋白的产生。美拉德反应在体内和体外都会发生，并且与糖尿病、衰老及与年龄相关疾病的慢性并发症有关。高血糖会导致葡萄糖的自氧化、蛋白质的糖基化以及多元醇代谢的激活。这些变化促进了活性氧的产生，并降低了抗氧化酶如铜锌超氧化物歧化酶的活性，导致氧化应激显著增加。大量证据表明线粒体改变参与其中，并在各种与氧化应激相关的疾病中起核心作用。受损的线粒体比正常线粒体产生更多的ROS（增加氧化应激）和更少的ATP（细胞能量）。由于它们受损，它们无法燃烧或利用葡萄糖或脂质，也无法为细胞提供ATP。此外，葡萄糖、氨基酸和脂质将无法被正确利用，并会在线粒体外积累；它们会经历更多的糖基化（如在糖尿病、肥胖症、HIV感染和脂肪营养不良中观察到的）。本文的目的是讨论如何阻止氧化应激、美拉德反应和线粒体之间形成的恶性循环。将讨论一些抗氧化剂通过靶向线粒体来减少糖基化现象并增强抗氧化防御系统的潜在应用。食品和制药公司面临同样的挑战，它们现在必须立即、积极有力地采取行动。
