Role of oxidative stress in development of cardiovascular complications in diabetes mellitus.
Diabetes represents a serious risk factor for the development of cardiovascular problems such as coronary heart disease, peripheral arterial disease, hypertension, stroke, cardiomyopathy, nephropathy and retinopathy. Identifying the pathogenesis of this increased risk provides a basis for secondary intervention to reduce morbidity and mortality in diabetic patients. Hyperglycemia and protein glycation, increased inflammation, a prothrombotic state and endothelial dysfunction have all been implicated as possible mechanisms for such complications. A linking element between many of these phenomena could possibly be, among other factors, increased production of reactive oxygen species. Vascular endothelial cells have several physiological actions that are essential for the normal function of the cardiovascular system. These include the production of nitric oxide (NO), which regulates vasodilatation, anticoagulation, leukocyte adhesion, smooth muscle proliferation and the antioxidative capacity of endothelial cells. However, under conditions of hyperglycemia, excessive amounts of superoxide radicals are produced inside vascular cells and this can interfere with NO production leading to the possible complications. This article aims at reviewing the links between reactive oxygen species, diabetes and vascular disease and whether or not antioxidants can alter the course of vascular complications in diabetic patients and animal models. A possible beneficial effect of antioxidants might present a new addition to the range of secondary preventive measures used in diabetic patients.
Haidara
Mohamed A
MA
Department of Physiology, Kasr Al-Aini Faculty of Medicine, Cairo University, Egypt. haidaram@hotmail.com
Yassin
Hanaa Z
HZ
Rateb
Moshira
M
Ammar
Hania
H
Zorkani
Mahmoud A
MA
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D001205:Ascorbic Acid / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D002986:Clinical Trials as Topic; D048909:Diabetes Complications / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D050171:Dyslipidemias / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors; D014810:Vitamin E / Q000494:pharmacology / Q000627:therapeutic use; D024502:alpha-Tocopherol / Q000494:pharmacology / Q000627:therapeutic use
D000975:Antioxidants; D017382:Reactive Oxygen Species; D014810:Vitamin E; D009569:Nitric Oxide; D024502:alpha-Tocopherol; D005947:Glucose; D001205:Ascorbic Acid