Membrane alteration as a basis of aging and the protective effects of calorie restriction.
As has been experimentally determined, oxidative modification to biological systems can be extensive, although the identification and stochiometric relation of the reactive species that cause these alterations have not been fully elucidated. In this review, arguments are presented to support the notion that the combined effects of membrane lipid peroxidation and its by-products, reactive aldehydes are likely responsible for membrane-associated functional declines during aging. As evidence for a systemic response to overall oxidative stress, the molecular inflammation hypothesis of aging is discussed by considering that the activation of inflammatory genes act as a bridge linking normal aging to pathological processes.
Yu
Byung Pal
BP
Department of Physiology, University of Texas Health Science Center, San Antonio, TX, USA. bpyu@earthlink.net
D000375:Aging; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D031204:Caloric Restriction; D002462:Cell Membrane / Q000473:pathology; D002149:Energy Intake; D004734:Energy Metabolism; D005609:Free Radicals; D006801:Humans; D007249:Inflammation; D015227:Lipid Peroxidation; D008055:Lipids / Q000737:chemistry; D008928:Mitochondria / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D017382:Reactive Oxygen Species
D000447:Aldehydes; D005609:Free Radicals; D008055:Lipids; D017382:Reactive Oxygen Species; D010100:Oxygen