ABSTRACT
Substantial in vitro and animal model evidence implicates the free radical-mediated oxidation of low density lipoprotein and its subsequent preferential uptake by macrophages in the arterial intima as an important factor in the development of vascular disease. In addition, antioxidants which prevent the oxidation of LDL in vitro also reduce the severity of vascular disease in animal models. Although some epidemiological studies also suggest that inadequate antioxidant status is related to the development of vascular disease, particularly cardiovascular disease, results from intervention trials have been contradictory. Whereas vitamin E may have a role in reducing the incidence of vascular disease, evidence is less strong for vitamin C, flavonoids and beta-carotene. Additionally, supplementation with some antioxidants such as beta-carotene may increase the incidence of cancer in high risk groups. Although increasing antioxidant intake is generally beneficial for health, this should perhaps be achieved by an increased dietary intake of antioxidant-rich foods rather than by use of supplements.
Subject(s)
Antioxidants/metabolism , Cardiovascular Diseases/etiology , Peripheral Vascular Diseases/etiology , Animals , Cardiovascular Diseases/metabolism , Female , Humans , Lipoproteins, LDL/metabolism , Male , Mice , Oxidation-Reduction , Peripheral Vascular Diseases/metabolism , Rabbits , Risk Factors , Vitamins/metabolismABSTRACT
Despite high plasma levels of vitamin E, red blood cell membranes contain relatively low levels of vitamin E. This suggests the existence of a selective vitamin E uptake/regeneration system in human red blood cell membranes. alpha-Tocopherol binding sites on human red blood cells are thought to be involved in the uptake of alpha-tocopherol from the plasma. To understand the role of the uptake system we have compared the alpha-tocopherol content and binding activity of red blood cells from smokers and non-smokers. The specific binding of [3H] alpha-tocopherol to pure red blood cell preparations from smokers (n = 7, 28.4 +/- 2.8 years) was 30.6 +/- 3.2 fmoles per 3 x 10(8) red blood cells and for non-smokers (n = 17, 27.9 +/- 1.3 years) was 41.7 +/- 3.7 fmoles per 3 x 10(8) red blood cells. Thus alpha-tocopherol uptake activity was significantly lower in smokers (P = 0.05). Red blood cells from smokers contained less (1.8 +/- 0.4 micrograms/gHb) alpha-tocopherol than non-smokers (2.8 +/- 0.3 micrograms/gHb), (P < 0.05), despite plasma levels of alpha-tocopherol being similar: 12.9 +/- 0.8 microM in non-smokers vs. 12.7 +/- 0.5 microM in smokers. However, adjusting plasma alpha-tocopherol for total plasma cholesterol plus triacylglycerols showed alpha-tocopherol levels were higher (P < 0.01) in non-smokers (2.84 +/- 0.10 mumol alpha-tocopherol/ mmol [cholesterol+triacylglycerol]) than in smokers (2.36 +/- 0.11 mumol alpha-tocopherol/mmol [cholesterol+triacylglycerol]). The reduced alpha-tocopherol levels in red blood cells from smokers may be due to impairment of alpha-tocopherol uptake activity. The reduced levels of alpha-tocopherol in smokers red blood cells was not associated with any changes in cell membrane fluidity. At present it is not known whether supplementation of smokers with vitamin E would normalise the alpha-tocopherol uptake activity of red blood cells.
Subject(s)
Erythrocytes/metabolism , Smoking , Vitamin E/metabolism , Adult , Antioxidants/analysis , Antioxidants/metabolism , Ascorbic Acid/blood , Ascorbic Acid/metabolism , Cholesterol/blood , Cholesterol, LDL/blood , Erythrocyte Membrane/metabolism , Female , Fluorescence Polarization , Humans , Lipid Peroxidation , Male , Vitamin E/blood , Vitamin E/pharmacokinetics , beta Carotene/blood , beta Carotene/metabolismABSTRACT
OBJECTIVE: To relate premature mortality from coronary heart disease (CHD) to national food and nutrient supplies. DESIGN: Descriptive correlational study. SETTING: Nineteen western European and five non-European countries. METHODS: Premature mortality from CHD in men below 65 years was related to recalculated Food and Agriculture Organization (FAO) food, antioxidant vitamins and other nutrient supply data in 24 developed countries for 1985-87. Longitudinal analyses of death rates from CHD and supplies between 1970 and 1987 were carried out for all the countries. Correlational analyses of supplies that preceded mortality by up to 10 years were also undertaken. RESULTS: In 17 western European countries the inter-country association of dairy product supply with CHD was of moderate strength (r = 0.5) and the principal saturated fatty acids derived from dairy products: butyric, caproic and myristic acids (C4:0, C6:0 and C14:0) were the most strongly related with CHD (r = 0.5, 0.5 and 0.4 respectively). The phenolic-antioxidant-rich foods, e.g. wine, vegetables and vegetable oils, were inversely related to CHD (r = -0.8, -0.7 and -0.6 respectively). Of the antioxidant vitamins, the alpha-tocopherol component of vitamin E was strongly related to CHD across Europe (r = -0.8). The major determinant of alpha-tocopherol supply was usually sunflowerseed oil. Vitamin C and beta-carotene gave moderate correlations (r = -0.6 and -0.5 respectively). Latency periods of 5 and 10 years between supplies and mortality rates did not markedly change the correlations. Longitudinal analyses of nutrient supplies and death rates within each country from 1970 to 1987 also showed that for the majority of countries there was an inverse association between supply of alpha-tocopherol and CHD. CONCLUSIONS: Dietary alpha-tocopherol may provide at least as good an explanation as does wine for the paradoxically low rates of CHD in several European countries which have a relatively high saturated fatty acid intake.