title: Free radicals and brain aging.
abstract: We reviewed here the formation of free radicals and its effect physiologically. Studies mentioned above have indicated that free radical/ROS/RNS involvement in brain aging is direct as well as correlative. Increasing evidence demonstrates that accumulation of oxidation of DNA, proteins, and lipids by free radicals are responsible for the functional decline in aged brains. Also, lipid peroxidation products, such as MDA, HNE, and acrolein, were reported to react with DNA and proteins to produce further damage in aged brains. Therefore, the impact of free radicals on brain aging is pronounced. It has been estimated that 10,000 oxidative interactions occur between DNA and endogenously generated free radicals per human cell per day, and at least one of every three proteins in the cell of older animals is dysfunctional as an enzyme or structural protein, due to oxidative modification. Although these estimated numbers reveal that free radical-mediated protein and DNA modification play significant roles in the deterioration of aging brain, they do not imply that free radical damages are the only cause of functional decline in aged brain. Nevertheless,although other factors may be involved in the cascade of damaging effects in the brain, the key role of free radicals in this process cannot be underestimated. This article has examined the role and formation of free radicals in brain aging. We propose that free radicals are critical to cell damage in aged brain and endogenous, and that exogenous antioxidants, therefore, may play effective roles in therapeutic strategies for age-related neurodegenerative disorders.
authors.affiliation: Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington 40506, USA.
authors.forename: H Fai
authors.initials: HF
authors.lastname: Poon
authors.forename: Vittorio
authors.initials: V
authors.lastname: Calabrese
authors.forename: Giovanni
authors.initials: G
authors.lastname: Scapagnini
authors.forename: D Allan
authors.initials: DA
authors.lastname: Butterfield
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D005609:Free Radicals; D015577:Geriatric Assessment; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D008297:Male; D009585:Nitrogen Dioxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D012106:Research; D012680:Sensitivity and Specificity
chemical_list: D005609:Free Radicals; D006360:Heat-Shock Proteins; D017382:Reactive Oxygen Species; D009585:Nitrogen Dioxide