Antioxidants and the Prevention of Coronary Heart Disease

Hoffman, Richard M.; Garewal, Harinder S.

doi:10.1001/archinte.1995.00430030025003

Cited by 60 publications

(13 citation statements)

References 58 publications

(1 reference statement)

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“…5,18,38 The literature suggests that LDL is primarily modified in the arterial wall because of the large antioxidant capacity of the blood. 39 However, recent data show that modification of LDL can occur in the blood. [13][14][15][16][17] Furthermore, prolonged LDL circulation times in the blood increase LDL's propensity to oxidation and may lead to LDL modification before it enters the artery wall.…”

Section: Discussionmentioning

confidence: 99%

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Gardner

Banka

Roberts

et al. 1999

ATVB

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Abstract-Current research suggests that estrogen may have primary effects on the artery wall. To investigate the mechanisms of female sex hormone actions in the artery wall, we used an isolated, perfused, rat carotid artery model to examine the effects of estradiol on the rates of accumulation of normal (N-LDL) and minimally modified (MM-LDL) low density lipoprotein in ovariectomized rats. N-LDL, MM-LDL, and oxidized LDL (OX-LDL) were fluorescently labeled and perfused into individual arteries. The rate of LDL accumulation was measured by quantitative fluorescence microscopy before and after treatment with estradiol (1 nmol/L, 272 pg/mL). Estradiol had no effect on the rate of Key Words: artery Ⅲ arteriosclerosis Ⅲ LDL Ⅲ estrogen Ⅲ oxidized LDL Ⅲ endothelium Ⅲ permeability A cardinal characteristic of the development of atherosclerosis is the accumulation of LDL within the arterial wall. 1-3 Sites of relative increase in LDL permeability have been identified in normal arteries 4 and can be induced by injury to the endothelium. 5-9 Alternatively, others have reported increased binding and decreased efflux of LDL from the vascular wall, even under conditions where LDL influx was not affected. 10,11 Therefore, LDL accumulation in the artery wall potentially occurs by several mechanisms, perhaps depending on the stage of atheroma formation.A large body of evidence indicates that modification of LDL in the artery wall promotes atherosclerosis. 12 Recent studies demonstrate evidence of modification of LDL in the blood. [13][14][15][16][17] Furthermore, a previous study showed increased accumulation and degradation of oxidized LDL (OX-LDL) in the artery wall in vivo. 18 These studies suggest that the reason there is increased accumulation and degradation of OX-LDL is because arterial permeability to undegraded, OX-LDL is greater than arterial permeability to native LDL (N-LDL). However, the precise mechanism(s) by which modified LDL (MM-LDL) affects LDL flux in the artery wall, such as increases in permeability to LDL, remains incompletely understood.Modification of LDL (eg, oxidation), either in the circulation or the artery wall, could promote atherosclerosis by increasing LDL accumulation in the artery. Also, alteration of constituents of the artery wall, such as proteoglycans, could influence LDL binding to the artery wall. Furthermore, oxidant-mediated injury of endothelial cell membranes could compromise the endothelial layer barrier to macromolecules in arteries. 5 To counteract oxidant stress effects on LDL and/or the artery wall, a number of potential antioxidants have been examined. In particular, some estrogens (eg, 17␤-estradiol) are known to reduce LDL accumulation in the artery wall 19,20 and to be potent antioxidants. [21][22][23] In addition, estrogens may protect endothelial cells from oxidative damage. 21,22 This action would be expected to prevent increased LDL permeation into the artery wall. Furthermore, estradiol has been shown to inhibit LDL oxidation in vivo at supraphysiological 24 and physiolo...

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Section: Discussionmentioning

confidence: 99%

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Gardner

Banka

Roberts

et al. 1999

ATVB

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“…Although the latter is mainly a public health issue concerning the degree of knowledge people have about CHD and the organization of health systems, the former is characterized by several questions that require more research. In this sense, further research on the use of antioxidants, particularly naturally occurring antioxidant vitamins such as vitamins E and C and β-carotene, seems to be a very promising field of investigation for the prevention of myocardial infarction (MI), progression of CHD, or stroke (4)(5)(6)(7)(8)(9)(10)(11)(12).…”

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confidence: 99%

Antioxidant vitamins and prevention of cardiovascular disease: Epidemiological and clinical trial data

Marchioli¹,

Schweiger

Levantesi³

et al. 2001

Lipids

151

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Naturally occurring antioxidants such as vitamin E, beta-carotene, and vitamin C can inhibit the oxidative modification of low density lipoproteins. This action could positively influence the atherosclerotic process and, as a consequence, the progression of coronary heart disease. A wealth of experimental studies provide a sound biological rationale for the mechanisms of action of antioxidants, whereas epidemiologic studies strongly sustain the "antioxidant hypothesis." To date, however, clinical trials with beta-carotene supplements have been disappointing, and their use as a preventive intervention for cancer and coronary heart disease should be discouraged. Only scanty data from clinical trials are available for vitamin C. As to vitamin E, discrepant results have been obtained by the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study with a low-dose vitamin E supplementation (50 mg/d) and the Cambridge Heart Antioxidant Study (400-800 mg/d). The results of the GISSI-Prevenzione (300 mg/d) and HOPE (400 mg/d) trials suggest the absence of relevant clinical effects of vitamin E on the risk of cardiovascular events. Currently ongoing are several large-scale clinical trials that will help in clarifying the role of vitamin E in association with other antioxidants in the prevention of atherosclerotic coronary disease.

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“…Phenolic compounds in red wine were suggested as one factor responsible for the "French paradox," the phenomenon of a lower incidence of cardiovascular diseases in France compared to matching European populations with similar exposure to risk factors (5,6). Besides cardiovascular diseases (7,8), phenolic compounds are believed to contribute positively to prevention of other degenerative malfunctions such as aging (9) and cancer (1,10,11). The mechanisms behind the different beneficial effects of dietary phenolic compounds are not fully elucidated, but these compounds are known to act as antioxidants (12,13), hypocholesterolemic (14,15) and enzyme-modulating agents (16)(17)(18) as well as phytohormones (19).…”

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confidence: 99%

Effects of dietary phenolic compounds on tocopherol, cholesterol, and fatty acids in rats

Kamal‐Eldin

Frank

Razdan

et al. 2000

Lipids

141

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The effects of the phenolic compounds butylated hydroxytoluene (BHT), sesamin (S), curcumin (CU), and ferulic acid (FA) on plasma, liver, and lung concentrations of alpha- and gamma-tocopherols (T), on plasma and liver cholesterol, and on the fatty acid composition of liver lipids were studied in male Sprague-Dawley rats. Test compounds were given to rats ad libitum for 4 wk at 4 g/kg diet, in a diet low but adequate in vitamin E (36 mg/kg of gamma-T and 25 mg/kg of alpha-T) and containing 2 g/kg of cholesterol. BHT significantly reduced feed intake (P < 0.05) and body weight and increased feed conversion ratio; S and BHT caused a significant enlargement of the liver (P < 0.001), whereas CU and FA did not affect any of these parameters. The amount of liver lipids was significantly lowered by BHT (P < 0.01) while the other substances reduced liver lipid concentrations but not significantly. Regarding effects on tocopherol levels, (i) feeding of BHT resulted in a significant elevation (P< 0.001) of alpha-T in plasma, liver, and lung, while gamma-T values remained unchanged; (ii) rats provided with the S diet had substantially higher gamma-T levels (P < 0.001) in plasma, liver, and lung, whereas alpha-T levels were not affected; (iii) administration of CU raised the concentration of alpha-T in the lung (P < 0.01) but did not affect the plasma or liver values of any of the tocopherols; and (iv) FA had no effect on the levels of either homolog in the plasma, liver, or lung. The level of an unknown substance in the liver was significantly reduced by dietary BHT (P < 0.001). BHT was the only compound that tended to increase total cholesterol (TC) in plasma, due to an elevation of cholesterol in the very low density lipoprotein + low density lipoprotein (VLDL + LDL) fraction. S and FA tended to lower plasma total and VLDL + LDL cholesterol concentrations, but the effect for CU was statistically significant (P < 0.05). FA increased plasma high density lipoprotein cholesterol while the other compounds reduced it numerically, but not significantly. BHT, CU, and S reduced cholesterol levels in the liver TC (P < 0.001) and percentages of TC in liver lipids (P < 0.05). With regard to the fatty acid composition of liver lipids, S increased the n-6/n-3 and the 18:3/20:5 polyunsaturated fatty acids (PUFA) ratios, and BHT lowered total monounsaturated fatty acids and increased total PUFA (n-6 + n-3). The effects of CU and FA on fatty acids were not highly significant. These results suggest some in vivo interactions between these phenolic compounds and tocopherols that may increase the bioavailability of vitamin E and decrease cholesterol in rats.

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Antioxidants and the Prevention of Coronary Heart Disease

Cited by 60 publications

References 58 publications

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Antioxidant vitamins and prevention of cardiovascular disease: Epidemiological and clinical trial data

Effects of dietary phenolic compounds on tocopherol, cholesterol, and fatty acids in rats

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