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Titolo:
Decreased thioredoxin and increased thioredoxin reductase levels in Alzheimer's disease brain
Autore:
Lovell, MA; Xie, CS; Gabbita, SP; Markesbery, WR;
Indirizzi:
Univ Kentucky, Sanders Brown Ctr Aging, Dept Chem, Lexington, KY 40536 USAUniv Kentucky Lexington KY USA 40536 , Dept Chem, Lexington, KY 40536 USA Univ Kentucky, Sanders Brown Ctr Aging, Dept Neurol, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 Dept Neurol, Lexington, KY 40536 USA Univ Kentucky, Sanders Brown Ctr Aging, Dept Pathol, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 Dept Pathol, Lexington, KY 40536 USA
Titolo Testata:
FREE RADICAL BIOLOGY AND MEDICINE
fascicolo: 3, volume: 28, anno: 2000,
pagine: 418 - 427
SICI:
0891-5849(20000201)28:3<418:DTAITR>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; OXIDATIVE DAMAGE; ENZYMATIC REDUCTION; PROTEIN DISULFIDES; REDOX CONTROL; STRESS; DNA; FLUID; CELLS; AP-1;
Keywords:
thioredoxin; thioredoxin reductase; oxidative stress; Alzheimer's disease; amyloid beta-peptide; free radicals;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Lovell, MA Univ Kentucky, Sanders Brown Ctr Aging, Dept Chem, 101 Sanders Brown Bldg,800 S Limestone St, Lexington, KY 40536 USA Univ Kentucky 101 Sanders Brown Bldg,800 S Limestone St Lexington KY USA 40536
Citazione:
M.A. Lovell et al., "Decreased thioredoxin and increased thioredoxin reductase levels in Alzheimer's disease brain", FREE RAD B, 28(3), 2000, pp. 418-427

Abstract

Increasing evidence supports the role of reactive oxygen species (ROS) in the pathogenesis of Alzheimer's disease (AD). Both in vivo and in vitro studies demonstrate that thioredoxin (Trx) and thioredoxin reductase (TR), theenzyme responsible for reduction of oxidized Trx, have protective roles against cytotoxicity mediated by the generation of ROS. The present study measured levels of Tn; protein and activities of TR in the brain in AD compared with control subjects, and evaluated the possible protective role of TR and Trx against amyloid beta-peptide (A beta) toxicity in neuronal cultures. Analysis of Trx; protein levels in 10 AD and 10 control subjects demonstrated a general decrease in all AD brain regions studied, with statistically significant decreases in the amygdala (p < .05), hippocampus/parahippocampal gyrus (p < .05), and marginally significant (p < .10) depletions in the superior and middle temporal gryi. Thioredoxin reductase activity levels were increased in all AD brain regions studied with statistically significant increases occurring in AD amygdala (p = .01) and cerebellum (p = .007). To investigate the protective effects of Trx and TR against A beta-induced toxicity, primary hippocampal cultures were treated with Trx or TR in combination with toxic doses of A beta. Treatment of cultures with Tn led to a statistically significant concentration-dependent enhancement in cell survival against A beta-mediated toxicity as did treatment with TR. Together, these data suggest that, although TR is protective against A beta-mediated toxicity, the increase observed in AD brain offers no protection due to the significant decrease in Trx levels. This decrease in the antioxidant Trx-TR system may contribute to the increased oxidative stress and subsequent neurodegeneration observed in the brain in AD. (C) 2000 Elsevier Science Inc.

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Documento generato il 03/07/20 alle ore 01:33:35