Abstract
Annual Review of Nutrition
Vol. 25:
151-174
(Volume publication date August 2005)
(doi:10.1146/annurev.nutr.24.012003.132446)
VITAMIN E, OXIDATIVE STRESS, AND INFLAMMATION ▪ Abstract Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Its incidence has also been increasing lately in developing countries. Several lines of evidence support a role for oxidative stress and inflammation in atherogenesis. Oxidation of lipoproteins is a hallmark in atherosclerosis. Oxidized low-density lipoprotein induces inflammation as it induces adhesion and influx of monocytes and influences cytokine release by monocytes. A number of proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) modulate monocyte adhesion to endothelium. C-reactive protein (CRP), a prototypic marker of inflammation, is a risk marker for CVD and it could contribute to atherosclerosis. Hence, dietary micronutrients having anti-inflammatory and antioxidant properties may have a potential beneficial effect with regard to cardiovascular disease. Vitamin E is a potent antioxidant with anti-inflammatory properties. Several lines of evidence suggest that among different forms of vitamin E, α-tocopherol (AT) has potential beneficial effects with regard to cardiovascular disease. AT supplementation in human subjects and animal models has been shown to decrease lipid peroxidation, superoxide (O2-) production by impairing the assembly of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase as well as by decreasing the expression of scavenger receptors (SR-A and CD36), particularly important in the formation of foam cells. AT therapy, especially at high doses, has been shown to decrease the release of proinflammatory cytokines, the chemokine IL-8 and plasminogen activator inhibitor-1 (PAI-1) levels as well as decrease adhesion of monocytes to endothelium. In addition, AT has been shown to decrease CRP levels, in patients with CVD and in those with risk factors for CVD. The mechanisms that account for nonantioxidant effects of AT include the inhibition of protein kinase C, 5-lipoxygenase, tyrosine–kinase as well as cyclooxygenase-2. Based on its antioxidant and anti-inflammatory activities, AT (at the appropriate dose and form) could have beneficial effects on cardiovascular disease in a high-risk population. Most recent citing papers (via CrossRef)Vitamin E status and quality of life in the elderly: influence of inflammatory processes British Journal of Nutrition:1 (2009) Systemic hypoxia enhances bactericidal activities of human polymorphonuclear leuocytes Clinical Science 116(11):805-817 (2009) Soy constituents: modes of action in low-density lipoprotein management Nutrition Reviews 67(4):222-234 (2009) Chromium supplementation enhances insulin signalling in skeletal muscle of obese KK/HlJ diabetic mice Diabetes, Obesity and Metabolism 11(4):293-303 (2009) Naringenin-Loaded Nanoparticles Improve the Physicochemical Properties and the Hepatoprotective Effects of Naringenin in Orally-Administered Rats with CCl4-Induced Acute Liver Failure Pharmaceutical Research 26(4):893-902 (2009)
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