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Titolo:
OXIDATIVE STRESS AND DIABETIC VASCULAR COMPLICATIONS
Autore:
GIUGLIANO D; CERIELLO A; PAOLISSO G;
Indirizzi:
VIA EMILIA 1 I-80021 AFRAGOLA NA ITALY UNIV NAPLES 2,DEPT GERIATR & METAB DIS NAPLES ITALY UNIV UDINE,DEPT CLIN & EXPT MED I-33100 UDINE ITALY
Titolo Testata:
Diabetes care
fascicolo: 3, volume: 19, anno: 1996,
pagine: 257 - 267
SICI:
0149-5992(1996)19:3<257:OSADVC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYDROXYL RADICAL PRODUCTION; LOW-DENSITY LIPOPROTEINS; HUMAN-ENDOTHELIAL CELLS; CORONARY HEART-DISEASE; VITAMIN-E CONSUMPTION; NITRIC-OXIDE; LIPID-PEROXIDATION; ELEVATED GLUCOSE; RISK-FACTORS; CARDIOVASCULAR MORTALITY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
151
Recensione:
Indirizzi per estratti:
Citazione:
D. Giugliano et al., "OXIDATIVE STRESS AND DIABETIC VASCULAR COMPLICATIONS", Diabetes care, 19(3), 1996, pp. 257-267

Abstract

Long-term vascular complications still represent the main cause of morbidity and mortality in diabetic patients. Although prospective randomized long-term clinical studies comparing the effects of conventionaland intensive therapy have demonstrated a clear link between diabetichyperglycemia and the development of secondary complications of diabetes, they have not defined the mechanism through which excess glucose results in tissue damage. Evidence has accumulated indicating that thegeneration of reactive oxygen species (oxidative stress) may play an important role in the etiology of diabetic complications. This hypothesis is supported by evidence that many biochemical pathways strictly associated with hyperglycemia (glucose autoxidation, polyol pathway, prostanoid synthesis, protein glycation) can increase the production of free radicals. Furthermore, exposure of endothelial cells to high glucose leads to augmented production of superoxide anion, which may quench nitric oxide, a potent endothelium-derived vasodilator that participates in the general homeostasis of the vasculature. In further supportof the consequential injurious role of oxidative stress, many of the adverse effects of high glucose on endothelial functions, such as reduced endothelial-dependent relaxation and delayed cell replication, arereversed by antioxidants. A rational extension of this proposed role for oxidative stress is the suggestion that the different susceptibility of diabetic patients to microvascular and macrovascular complications may be a function of the endogenous antioxidant status.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/08/20 alle ore 20:34:42