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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate the effects of large amounts of dietary vitamin E and butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in rabbits fed a low-cholesterol, atherogenic diet, and to seek for evidence of lipid peroxidation in the atherosclerotic lesions. Rabbits were fed a purified atherogenic diet, containing butter or the basal diet supplemented with either 1.0% of vitamin E or 0.1% each of BHA and BHT for periods up to 3 years; a negative control group was fed the basal diet with corn oil replacing butter. Aortic and coronary atherosclerosis were more frequent and extensive in rabbits fed either the basal diet or the basal diet supplemented with BHA and BHT than in rabbits fed either the basal diet supplemented with vitamin E or the negative control diet. Dietary vitamin E inhibited atherogenesis by preventing hypercholesterolemia. No evidence of lipid peroxidation was detected in the arterial lesions.
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PMID:Vitamin E, antioxidants and lipid peroxidation in experimental atherosclerosis of rabbits. 71 30

Rabbits were fed diets including cholesterol and 10% butterfat to determine whether polyunsaturated butter (9% 18:2) would be less atherogenic than normal saturated butter (3% 18:2) when fed for 12 weeks. The cholesterol diets alone, 0.5% or 2%, produced aortic plaque development, and plasma cholesterol increased 20 times, lipids increased 10 times, and vitamin E increased 5 times. The inclusion of both fat and cholesterol in the diet produced a synergistic effect, doubling these values to 40 times for cholesterol, 20 times for lipids, and 10 times for vitamin E. The higher circulating levels of cholesterol caused increased tissue levels of cholesterol. With 2% cholesterol and fat, liver and aorta cholesterol increased 10 times, heart 4 times, and muscle cholesterol 2 times. The lower 0.5% dietary cholesterol load was successful in limiting the amount of tissue cholesterol increase. Liver, aorta, heart, and muscle levels of cholesterol were only about half the concentration attained when 2% cholesterol was fed. It was concluded that there were no differences in plasma or tissue cholesterol, vitamin E, or atherosclerosis attributable to the polyunsaturated nature of the diet. The 10% butterfat diets alone, whether saturated or unsaturated, did not induce aortic plaques and did not increase blood or tissue cholesterol, lipids, or vitamin E. Our results suggest that the lipid mobilizing effect is mediated by cholesterol, probably by conversion to bile acids and a stimulation in intestinal absorption.
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PMID:Vitamin e, cholesterol, and lipids during atherogenesis in rabbits. 93 22

Marked hypercholesterolemia and moderate lipid infiltration of the aorta were induced by feeding rabbits a diet containing 1% cholesterol + 3% corn oil for 70 days. In the liver the concentration and pool size of cholesterol increased and those of triglycerides (TG) decreased. On dietary addition of vitamin A and vitamin E (44 000 I.U. and 125 mg respectively, once daily for 5 days a week) the following changes were noted in comparison with the fat-fed rabbits not receiving extra addition of vitamins. There was a slight decrease of the levels of plasma cholesterol and an increase of those of plasma TG. The liver cholesterol concentration increased but, according to the concomitant reduction of the liver weight, there was no significant change in lever cholesterol or TG pools. In the aorta the vitamins markedly reduced the lipid infiltrated area as well as the cholesterol content. Both niceritrol** and S-2040 [pyridine-2,5-dicarboxylic acid di(beta-pyridylcarbinol ester)] in a dietary concentration of 0.5% decreased plasma cholesterol by about 20%. This reduction, as well as that induced by the vitamins, was confined to the VLDL-fractions only. S-2040 slightly reduced the cholesterol accumulation in the aorta. In rabbits given both the vitamins and niceritrol or S-2042 there was an additive reduction of plasma cholesterol. Here the nicotinic acid derivatives were partly able to counteract the increases of plasma TG induced by the vitamins. In the aorta the combination vitamins + S-2042 but not that of vitamins + niceritrol tended to give a better protection than the vitamins alone. On a normal diet vitamins A + E significantly increased the liver cholesterol concentration and pool and decreased the liver TG pool, but did not affect the other parameters. Possible mechanisms for the prophylactic action of the vitamins against lipid infiltration of the aorta of cholesterol-fed rabbits are discussed.
Atherosclerosis
PMID:Actions of vitamins A and E and some nicotinic acid derivatives on plasma lipids and on lipid infiltration of aorta in cholesterol-fed rabbits. 115 70

The effect of Hippophae rhamnoides on hyperlipidemic rabbit serum (HRS) cultured smooth muscle cells (SMC) was observed in comparison with vitamin E(VE). The results show that Hippophae rhamnoides, much like VE, is also a potent antioxidant. It strongly decreases the MDA content in HRS cultured SMC and protect the cells from the injury of lipid peroxidation, and thus keeps the SMC growing and proliferating health. The results implicate that Hippophae rhamnoides is an effective antioxidant, and one of the important mechanisms of Hippophae rhamnoides in anti-atherosclerosis reported recently may be closely related to the action of anti-lipid peroxidation.
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PMID:[The protective effect of Hippophae rhamnoides L. on hyperlipidemic serum cultured smooth muscle cells in vitro]. 129 83

The effects of vitamin E on the progress of atherosclerosis in patients on hemodialysis was investigated clinically using ACI. There was a significant suppression of the increase in ACI in group A, compared to group B, at the time of observation in each year. On the other hand, no significant changes were noted in BWD, CTR, BP and blood chemical examination, except that the level of MDA was significantly decreased in group A as compared with that in group B 4 years later. Since ACI is an index representing atherosclerosis, the results of this study seemed to suggest that the progress of atherosclerosis was suppressed by long-term administration of vitamin E in patients on hemodialysis.
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PMID:Prevention of aortic calcification in patients on hemodialysis by long-term administration of vitamin E. 129 37

Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.
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PMID:Tropical oils: nutritional and scientific issues. 134 19

Although primarily used as a lipid lowering drug, probucol also possesses anti-oxidant activity and has been shown in animal models to inhibit or delay the progression of atherosclerosis. It has been suggested that this anti-atherosclerotic effect may occur through inhibition of free radical oxidation of low density lipoprotein. The aim of this study was to investigate the effects of probucol on free radical activity in hyperlipidaemic patients. Plasma lipid peroxides were measured before probucol treatment, at 4 and 12 weeks treatment and then 4 weeks after stopping probucol. Lipid peroxide concentrations were significantly reduced during and 4 weeks after stopping treatment with probucol, when compared with baseline values. There were no changes in plasma vitamin E concentrations. The results of this study indicate that probucol reduces lipid peroxidation in patients, an effect which may occur through a free radical scavenging action.
Atherosclerosis 1992 Nov
PMID:Probucol reduces plasma lipid peroxides in man. 144 94

There is accumulating evidence that free radicals may contribute to various diseases such as cancer or cardiovascular disease. Possible health hazards can to some extent be prevented by the body's multilevel defense system against free radicals, which comprises, besides others, antioxidant vitamins. The 12-year mortality follow-up of 2,974 participants of the Basal Study allowed to test the hypothesis that low antioxidant vitamin plasma concentrations (vitamin A, C, E and carotene) were associated with increased death from cancer of various sites and death from atherosclerosis such as ischemic heart disease and stroke, respectively. For the analysis 204 cancer cases, 132 fatalities from ischemic heart disease (IHD) and 31 deaths from cerebral vascular disease were available. Cancer mortality. Overall mortality from cancer was associated with low mean plasma levels of carotene adjusted for cholesterol (p less than 0.01) and of vitamin C (p less than 0.01). Bronchus and stomach cancers were associated with a low mean plasma carotene level (p less than 0.01). Subjects with subsequent stomach cancer had also lower mean vitamin C and lipid-adjusted vitamin A levels than survivors (p less than 0.05). Calculating the relative risk with exclusion of mortality during the first two years of follow-up, low plasma carotene was associated with an increased risk for bronchus cancer (RR 1.8, p less than 0.05), and the small number of stomach cancer cases (RR 2.95, p less than 0.05) low plasma levels of carotene and vitamin A with all cancer types (RR 2.47, p less than 0.01), and low plasma retinol in older subjects (greater than 60 years) with lung cancer (RR 2.17, p less than 0.05). Studies in other cohorts with a poor vitamin E status revealed an increased risk of subsequent cancer at low vitamin E levels as well. It is concluded that low plasma levels of all major essential antioxidants are associated with an increased risk of subsequent cancer mortality. Cardio-vascular mortality. Plasma carotene concentration below quartile 1 was associated with an increased risk for IHD (RR 1.53, p = 0.02). The same was true for low levels of both carotene and vitamin C (RR = 1.96, p = 0.022). The risk of cerebrovascular death was elevated in subjects with low carotene in the presence of low vitamin C plasma concentration (RR 4.17, p less than 0.01). These data confirm and extend recent findings on an inverse correlation of beta-carotene and vitamin C respectively to CVD.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inverse correlation between essential antioxidants in plasma and subsequent risk to develop cancer, ischemic heart disease and stroke respectively: 12-year follow-up of the Prospective Basel Study. 145 Jun

Uptake of oxidatively modified low-density lipoprotein (LDL) by cells in the arterial wall is believed to be an important early event in the development of atherosclerosis. Because vitamin E is the major antioxidant present in human lipoproteins, it has received much attention as a suppressor of LDL lipid oxidation and as an epidemiological marker for ischaemic heart disease. However, a careful examination of lipid peroxidation in LDL induced by a steady flux of aqueous peroxyl radicals has demonstrated that, following consumption of endogenous ubiquinol-10, the rate of peroxidation (i) declines as vitamin E is consumed, (ii) is faster in the presence of vitamin E than following its complete consumption, (iii) is substantially accelerated by enrichment of the vitamin in LDL, either in vitro or by diet, and (iv) is virtually independent of the applied radical flux. We propose that perodixation is propagated within lipoprotein particles by reaction of the vitamin E radical (i.e. alpha-tocopheroxyl radical) with polyunsaturated fatty acid moieties in the lipid. This lipid peroxidation mechanism, which can readily be rationalized by the known chemistry of the alpha-tocopheroxyl radical and by the radical-isolating properties of fine emulsions such as LDL, explains how reagents which reduce the alpha-tocopheroxyl radical (i.e. vitamin C and ubiquinol-10) strongly inhibit lipid peroxidation in vitamin E-containing LDL.
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PMID:Vitamin E in human low-density lipoprotein. When and how this antioxidant becomes a pro-oxidant. 146 40

In the present study performed on rats, we investigated the influence of an in vivo acute iron load on several platelet parameters and their modification after vitamin E supplementation. Iron load was achieved by injecting iron dextran corresponding to 0.1 mg Fe3+ per kg in the gluteus muscles. Control rats were injected with an equal amount of a dextran solution. Analyses were performed 18 h after injection. By comparison with controls, in iron-injected animals, we found significant increases of: (1) serum total iron (by 110%); (2) aggregation of isolated platelets induced by low concentration of thrombin and ADP (by 350% and 120%, respectively); (3) thrombin-induced endogenous serotonin secretion (by 94%). We also studied the mobilization of radiolabeled arachidonate preincorporated into platelet phospholipids. The results indicated that the thrombin-stimulated release of arachidonate and formation of cyclooxygenase and lipoxygenase products (particularly thromboxane B2), were significantly increased. We also found in plasma an increase (by 67%) of malondialdehyde (MDA) as well as a decrease of vitamin E (by 60%). When vitamin E was injected the day before iron injection, platelet hyperactivity and thromboxane biosynthesis were reduced as well as the plasma MDA concentration. Consequently, given the key role of calcium flux in the activation processes in platelets, we also investigated the thrombin-induced Ca2+ uptake by means of radiocalcium. We found that in platelets from iron-treated rats the Ca2+ uptake amounted to 3670 +/- 201 pmol/10(9) platelets (plt) and was significantly different from controls (1680 +/- 192 pmol/10(9) plt, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1992 Oct
PMID:Effect of vitamin E on acute iron load-potentiated aggregation, secretion, calcium uptake and thromboxane biosynthesis in rat platelets. 146 49


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