Aging and glycoxidant stress.
Aging and related diseases are accompanied by increased Oxidative Stress (OS) and accumulation of Advanced Glycation End products (AGEs). One important component of AGEs accumulation with aging appears to be the sustained exposure to dietary AGE (dAGEs), which contributes to overloading of anti-AGE receptors and depletion of anti-oxidant reserves. In this review, we present experimental animal and human data which support this postulation. Lowering the content of AGEs in the normal diet significantly prevents AGEs accumulation and the increased OS caused by aging and also extends lifespan in mice. In humans, short-term trials indicate that a Low AGEs diet reduces oxidant burden and inflammatory markers. Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies.
Peppa
Melpomeni
M
Endocrine Unit, 2nd Dept of Internal Medicine-Propaedeutic, Research Institute and Diabetes Center, Athens University, Medical School, Athens, Greece. molypepa@otenet.gr
Uribarri
Jaime
J
Vlassara
Helen
H
D000368:Aged; D000375:Aging / Q000378:metabolism*; D000818:Animals; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*
D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic