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

After 30 days of bezafibrate administration to 5 patients with hypertriglyceridaemia and hyperapobetalipoproteinaemia a rise was found in the concentrations of cholesterol and vitamin E in the LDL fraction. In consequence the susceptibility of the LDL fraction to oxidation by macrophages was reduced. The uptake of modified LDL by these cells was decreased in relation to the uptake before treatment.
Atherosclerosis 1989 Oct
PMID:Modification of low density lipoproteins from hypertriglyceridemic patients by macrophages in vitro and the effect of bezafibrate treatment. 962 88

Age is strongly correlated to the onset of atherosclerotic lesion formation in humans. This may be associated with an age-related increase in the susceptibility of the vascular endothelium to oxidative injury. Such injury may result in altered endothelial function as a barrier to plasma components, such as cholesterol-rich lipoprotein remnants. To investigate this hypothesis, the relationship between endothelial cell culture age, susceptibility to oxidative injury and protection against this injury by the nutrient/antioxidant vitamin E on endothelial barrier function (transfer of albumin across endothelial monolayers) was examined. An acute 24 h exposure to 30 microM linoleic acid hydroperoxide resulted in increased albumin transfer at all cell passages tested (up to passage 50). Pre-enrichment of cells with 25 microM vitamin E always protected endothelial cells against oxidized fatty acid-induced cell injury, independent of cell age. In comparison, patterns of total cell protein and DNA were not markedly influenced by experimental treatments, although age-related declines in total DNA were noted. These data suggest that the possible correlation between age and the onset of atherosclerosis may be in part related to a decrease in endothelial barrier function due to oxidative stress, permitting more blood components to enter the arterial wall. Furthermore, vitamin E may protect endothelial cells against oxidant-mediated vascular injury.
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PMID:Protective effects of vitamin E in age-related endothelial cell injury. 259 93

An increased lipid peroxides and a decreased production of prostacyclin have been shown in advanced atherosclerotic lesions and plasma. Our purpose was to determine whether the similar findings could be observed in cultured endothelial cells, and whether antioxidants could protect the cell against peroxide injury. In these experiments we have used bovine aortic endothelial cells in culture to address the issue of hyperlipidemia-induced arterial damage. Results of the present study showed that different concentration of hyperlipidemic sera from atherogenic rabbits induced a time- and dose-dependent alteration in the production of prostacyclin and levels of lipid peroxides in endothelial cells. Endothelial cells incubated with hyperlipidemic serum increased prostacyclin generation significantly during the initial stages and then continuously decreased. When endothelial cells were incubated for 36 h, TXA2 generation was also impaired and at the same time the cellular lipid peroxides content increased. There was a positive correlation between the concentration of hyperlipidemic serum and lipid peroxides and an inverse correlation with prostacyclin synthesis. The medium supplemented with antioxidant selenium or vitamin E showed a significant decrease in lipid peroxides and an increase in prostacyclin synthesis. These results suggest that both hyperlipidemic serum and lipid peroxides injury endothelial cells and inactivate prostacyclin synthetase, resulting in a decrease of prostacyclin production, while antioxidants have a protective effect. We conclude that the increase in lipid peroxides in association with hyperlipidemia results in alteration of prostacyclin synthesis that may play an important role in the pathogenesis of atherosclerosis.
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PMID:Effect of hyperlipidemic serum on lipid peroxidation, synthesis of prostacyclin and thromboxane by cultured endothelial cells: protective effect of antioxidants. 267 46

Restricted ovulator hens, which develop hyperlipidemia, were fed 1000 IU vitamin E per k of diet. These hens maintained their hyperlipidemia but plasma peroxide levels were reduced to those of laying hens. The intimal thickness of the aorta was measured by light microscopy. Hyperlipidemic hens which had high plasma peroxide levels had an increased intimal thickness as compared to laying hens. Hyperlipidemic hens which had their plasma peroxide levels reduced by dietary vitamin E had intimal thicknesses the same as laying hens. It is suggested that hyperlipidemia without lipid peroxidation either does not promote atherogenesis or does so at a reduced rate.
Atherosclerosis 1989 Feb
PMID:Effect of dietary vitamin E on plasma lipids and atherogenesis in restricted ovulator chickens. 271 55

Plasma vitamin E, HDL-cholesterol, apolipoprotein B and triglycerides were measured in an apparently healthy, male, random population sample (n = 74) from Southern Italy. Plasma vitamin E concentration was positively correlated to that of serum cholesterol, non-HDL cholesterol, triglycerides and apolipoprotein B (all P less than 0.001). The results of partial correlation analysis showed that apo B, the apolipoprotein constituent of LDL, was related to vitamin E independently of serum triglycerides, a fairly accurate marker of VLDL. On the other hand, triglycerides were related to vitamin E independently of apo B. Both correlations were much weaker if an adjustment was performed for non-HDL-cholesterol. No independent relationship was demonstrated between plasma vitamin E and HDL-cholesterol.
Atherosclerosis 1989 May
PMID:Plasma vitamin E, apolipoprotein B and HDL-cholesterol in middle-aged men from southern Italy. 271 59

Peroxidation of lipoproteins has received attention recently in connection with its possible initiation and propagation of atherosclerosis. We studied indices of lipid peroxidation in plasma of 30 patients with either hypercholesterolemia or both hypercholesterolemia and hypertriglyceridemia, and compared them with those of 19 healthy subjects. In the patients lipid hydroperoxides measured both iodometrically and as thiobarbituric acid-reactive substances (TBA-RS) were significantly increased, while concentrations of thiol groups remained unchanged. There was no correlation between concentrations of hydroperoxides and TBA-RS, possibly because the two methods assessed different breakdown products of lipid peroxidation. Lipid hydroperoxide levels, but not those of TBA-RS were correlated with LDL-cholesterol and triglyceride levels. In 6 patients administration of vitamin E at a daily dosage of 300 mg for 4 to 6 weeks depressed elevated hydroperoxides by 33%, and TBA-RS by 44% on average.
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PMID:Incides of lipid peroxidation in patients with hypercholesterolemia and hypertriglyceridemia. 275 Jan 70

A new technique was elaborated for measuring LDL uptake by rat aortic endothelial cells in vivo, using a fluorescent marker (Dil)-labelled LDL and quantifying the fluorescence in cells selectively removed from the aorta. This technique was used to study the endothelial uptake of LDL modified by activated human monocytes (LDL-A) in comparison with native LDL (LDL-N) protected from oxidation by vitamin E during the preparation. Incubation of LDL with activated monocytes increased endothelial uptake in vivo by 9.3-fold and also by 4.4-fold in cultured confluent porcine endothelium. In contrast, only a 1.5-fold increase in uptake of LDL-A was observed in sparse cultures. Cytotoxicity of monocyte-altered or native LDL did not differ as measured by the [3H]deoxyglucose-release test on cultured endothelium. Our results suggest that modification of LDL in the circulation by monocytes may make an important contribution to atherogenesis.
Atherosclerosis 1987 May
PMID:Increased uptake of monocyte-treated low density lipoproteins by aortic endothelium in vivo. 303 35

Plasma low density lipoprotein (LDL) can undergo free radical oxidation either catalyzed by divalent cations, such as Cu2+ or Fe2+ or promoted by incubation with cultured cells such as endothelial cells, smooth muscle cells and monocytes. The content of vitamin E, beta-carotene and unsaturated fatty acids is decreased in oxidized LDL. A breakdown of apolipoprotein-B (apoB), hydrolysis of the phospholipids, an increase of thiobarbituric acid reactive substances and the generation of aldehydes also occur. Changes in the ratio of lipid to protein, the electrophoretic mobility and the fluorescent properties have also been reported to accompany oxidation of this lipoprotein. The functional changes of oxidized LDL include its recognition by the scavenger receptor on macrophages, its cytotoxicity especially to proliferating cells, its chemotactic properties with respect to monocyte-macrophages and its regulation of platelet-derived growth factor-like protein (PDGFc) production by endothelial cells. In this article we summarize some of the contributions to this topic and present speculations relating oxidized LDL to pathological conditions such as atherosclerosis.
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PMID:Modification of human serum low density lipoprotein by oxidation--characterization and pathophysiological implications. 331 31

Cholesterol oxidation products (oxysterols) found in foods may be atherogenic, possibly by altering the barrier function of the vascular endothelium. To investigate this hypothesis, endothelial cells were cultured on micropore filters and the effect of cholesterol and the oxysterol cholestan-3 beta,5 alpha,6 beta-triol (Triol) on albumin transfer across cultured vascular endothelial monolayers (ECM) was studied. Exposure to Triol significantly increased albumin transfer across ECM. The effect of Triol on endothelial cell barrier function was time and concentration dependent, with maximum albumin transfer being reached at 20 microM Triol and after a 24-h exposure. Pure cholesterol, on the other hand, did not affect albumin transfer at concentrations as high as 130 microM. Although an increase in albumin transfer across ECM was observed after a 2-h incubation with Triol-enriched media, a 24-h incubation period was necessary to cause a significant release of cellular lactate dehydrogenase (LDH) into the culture media. Morphological perturbations of the cell monolayers were observed at approx. 14-18 h after cell exposure to Triol-enriched media. Enrichment with cholesterol or vitamin E did not prevent the Triol-induced increase in albumin transfer across ECM. These results suggest that exposure to oxidized cholesterol, but not cholesterol, itself, reduces the ability of the endothelium to act as a selectively permeable barrier to plasma components, and that these events may not be prevented by cholesterol or vitamin E.
Atherosclerosis 1987 Dec
PMID:Cholestan-3 beta,5 alpha,6 beta-triol decreases barrier function of cultured endothelial cell monolayers. 342 58

This report describes measurements of 50 variables in adult, female, reproductively inactive Vervet monkeys during prolonged nutrition realistic for westernized people. Dietary treatments consisted of an atherogenic Western diet (WD) and a prudent Western diet (PD). Ingredients were normal foods for man and no extra cholesterol was added. Fortification of both diets with vitamin C after cooking was necessary to prevent deficiency. Randomised groups of Vervet monkeys received either the PD or WD for 47 months, while a third group was fed WD for 20 months and then PD for 27 months (WD-PD). Before the dietary treatments nourishment was by a high carbohydrate diet (HCD) and baseline and reference values (RV) apply to this nutritional status. Plasma total cholesterol (mg/dl) was increased from 147 (HCD) to 174 (PD) and 376 (WD). Individual cholesterolaemio response ranged from mild to severe and was stable (PD and WD). Dietary reversal (WD-PD) reduced cholesterolaemia promptly. Statistically significant increases in calcium, zinc and vitamin E and decreased vitamin B6 were associated with the WD relative to the PD (in serum and plasma). Two cholesterol metabolising microsomal enzymes in liver were notably increased and one unchanged (WD). There were no dietary effects on triglycerides, vitamin A and glucose in plasma; insulin, glucagon, electrolytes, copper, magnesium or enzymes reflecting liver, muscle or brain cell damage in serum. Red blood cells, platelets and directly associated parameters increased (WD), haemoglobin was the same and haemoglobin per red cell decreased. Bleeding time was not affected. Bivariate correlations across the diets confirmed that Western nutrition promoted inherent individual susceptibility to cholesterolaemia. There were notable differences from RVs in total cholesterol, calcium, packed cell volume and haemoglobin, which emphasise excesses and deficiencies of the WD and PD.
Atherosclerosis 1987 Aug
PMID:Diets realistic for westernized people significantly effect lipoproteins, calcium, zinc, vitamins C, E, B6 and haematology in vervet monkeys. 363 58


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