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

Selenium is an essential component of glutathione peroxidase, an enzyme which protects cells against peroxidation and controls concentrations of intracellular peroxides. Since selenium deficiency is clinically associated with an increased degree of atherosclerosis, the effects of selenium deficiency on prostacyclin (PGI2) and platelet activating factor (PAF) production by cultured human umbilical vein endothelial cells (HUVEC) were investigated. In selenium-deficient HUVEC, histamine-induced PGI2 synthesis was significantly decreased when compared to selenium-supplemented HUVEC; in contrast, histamine-induced PAF production was increased by selenium deficiency. Histamine-induced inositol trisphosphate and [Ca2+]i responses and the conversion of PGG2 and PGH2 to PGI2 were not altered by selenium deficiency. However, selenium deficiency decreased the conversion of exogenous arachidonate to PGI2 and markedly suppressed glutathione peroxidase activity. These results suggest that selenium deficiency, by decreasing glutathione peroxidase activity, makes HUVEC susceptible to peroxide-induced inhibition of the cyclooxygenase activity of PGH2 synthase, resulting in decreased PGI2 production. These changes may alter platelet function in vivo and thus play a role in the increased incidence of atherosclerosis reported in selenium-deficient individuals.
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PMID:Selenium deficiency inhibits prostacyclin release and enhances production of platelet activating factor by human endothelial cells. 251 81

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

Selenium deficiency has established implications in cardiovascular diseases, particularly on cardiac muscle integrity. The essential trace element takes part not only in the direct protection of endothelial cells against the accumulation of aggressive oxygen species, but also in the biosynthesis of arachidonic acid derivatives involved in platelet and leucocyte functions, or in the regulation of cholesterol. Moreover, it prevents toxic effects of cadmium and mercury, and modulates the active transport of calcium. Some clinical investigations have underlined its importance in the cardiac function and the prevention of coronary atherosclerosis, and several recent prospective epidemiological studies have attributed to selenium deficiency a greater incidence of cardiovascular diseases. Further studies should be devoted to the influence of marginal deficiency in this trace element whose optimal requirement does not seem to be met by the usual dietary intake.
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PMID:[Selenium and cardiovascular pathology]. 269 67

In a cross-sectional population study of 1132 unselected Eastern Finnish men aged 54 years, serum selenium concentration had a weak positive association with plasma HDL cholesterol (standardised partial regression coefficient, beta = 0.061, P = 0.019) and a fairly strong inverse relationship (beta = -0.223, P less than 0.001) with the extent of ADP-induced platelet aggregation. Neither plasma ascorbate concentration nor alpha-tocopherol to total cholesterol ratio had any association with plasma lipoproteins, platelet aggregability or prevalent ischaemic heart disease (IHD). When a covariance-correction was applied, men with ischaemic ECG findings at exercise had a lower mean serum selenium than others (81.5 micrograms/l vs. 85.9 micrograms/l, P less than 0.01 for difference). This difference was equally large for men with neither symptoms nor previous diagnosis of IHD.
Atherosclerosis 1988 Mar
PMID:Relationship of serum selenium and antioxidants to plasma lipoproteins, platelet aggregability and prevalent ischaemic heart disease in Eastern Finnish men. 325 19

The epidemiological and historical aspects of some important and representative wildlife diseases from Scandinavia are discussed. In noninfectious diseases, examples include cataract in moose (Alces alces), atherosclerosis in hybrid hares (Lepus timidus X L. europaeus), and ethmoid tumors in moose. The epizootiological and historical aspects of the recent epizootics of myxomatosis in European rabbits (Oryctolagus cuniculus) and rabies and sarcoptic mange in red foxes (Vulpes vulpes) are reviewed. The decline and subsequent increase in population abundances of tetraonids including the capercaillie (Tetrao urogallus), black grouse (Lyrurus tetrix), and hazel hen (Tetrastes bonasia) are discussed, and an hypothesis on predation by foxes is presented as a possible explanation for these population fluctuations. The potential impact of environmental pollution on wildlife populations is emphasized with reference to mercury in wildlife from Sweden and the possible effects of cadmium and selenium resulting from acidification. A bibliography of important references is presented pertaining to these and other diseases of wildlife from Scandinavia.
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PMID:A review of wildlife diseases from Scandinavia. 331 19

Selenium concentrations have been measured in plasma and in blood leucocytes from 29 haemodialysis patients and from 25 healthy men. The selenium contents of the plasma and white blood cells of the dialysis patients were significantly reduced (p less than 0.001). Selenium deficiency in humans results in a congestive cardiomyopathy and is associated with increased risks of accelerated atherosclerosis and cancer. Each of these is found with abnormal frequency in haemodialysis patients.
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PMID:Reduced plasma and white blood cell selenium levels in haemodialysis patients. 359 19

A dietary survey was conducted in 1980 in connection with the Multicentre Study on Atherosclerosis Precursors in Finnish Children in five urban and 12 rural communes in various parts of Finland. 1,768 children aged 3, 6, 9, 12, 15 and 18 years were interviewed using the 48 hour recall method. Food consumption, and the intakes of energy and 49 nutrients were calculated. The intakes of energy and most nutrients increased in the successive age groups until the age of 15 years. There were only small differences in the diet of children belonging to different social classes. Protein accounted for 14% of total energy intake, fat for 38%, total carbohydrate for 48%, and sucrose for 10%. The ratio of polyunsaturated and saturated fatty acids in the diet (P/S) was 0.24 for the whole material, which is higher than found in previous studies in Finland. The P/S ratio was higher in urban areas and West Finland than in rural areas and in East Finland. The share of fat of energy intake exceeded the recommendation given by the Ministry of Health and the P/S ratio was lower than recommended. The mean daily intakes of energy and vitamins met the recommendations. Of the mineral elements, the intakes of calcium, phosphorus, potassium, magnesium and manganese were abundant. The intakes of iron, copper, zinc, molybdenum and chromium were lower than recommended in most age groups and the intakes of selenium and fluorine in all age groups. The large share of refined foods in the children's diet was the main reason for the low nutrient densities.
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PMID:Atherosclerosis precursors in Finnish children and adolescents. VIII. Food consumption and nutrient intakes. 386 23

Male rats were fed a selenium-deficient Torula yeast diet with or without 0.2 ppm selenium (as sodium selenite) in the drinking water. Selenium deficiency caused a significant increase of urinary acetoacetate excretion in fed rats, and 24 or 48 hours of starvation enhanced this effect. Two days of selenium supplementation decreased the amount of urinary acetoacetate and 3-hydroxybutyrate to 50% of the deficiency value, indicating an enzymatic impairment in the selenium-deficient rat. No selenium-dependent effect was found for the following: (1) urinary pH, amount of nitrite, glucose (negative), hemoglobin or protein, and the urine was negative for phenylketones; (2) blood content of glucose, acetoacetate, or 3-hydroxybutyrate; or (3) liver content of glycogen, glucose, acetoacetate, or 3-hydroxybutyrate. On the other hand, the liver content of triglycerides was significantly lower in selenium deficiency. Indications for a higher content of ketone bodies (acetoacetate plus 3-hydroxybutyrate) in the kidneys from selenium-deficient rats were found. The increased urinary excretion of ketone bodies on selenium deficiency may indicate an impairment of lipid and ketone body turnover (in the kidney), or a decreased kidney reabsorption rate. Possible implications of these results in connection with protective roles of selenium in atherosclerosis and carcinogenesis are suggested.
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PMID:Impaired ketone body metabolism in the selenium deficient rat. Possible implications. 405 13

A prospective epidemiological study (Lancet ii: 175-179, 1982) implicates low concentrations of selenium in plasma in coronary atherogenesis. We examined this relationship more directly by fluorometry of selenium in the plasma of 91 hospitalized patients who were being examined by coronary arteriography for clinical evaluation of chest pain. We observed a significant, inverse correlation between the plasma selenium and severity of coronary atherosclerosis. These results confirm those of the epidemiological studies, but the role, if any, of selenium in atherogenesis still is unclear. Its concentration in plasma is decreased by ethanol and cigarette use; possibly this is the mechanism of its relation to hypertension and atherosclerosis.
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PMID:Selenium concentrations in plasma of patients with arteriographically defined coronary atherosclerosis. 673 2

Although there is no evidence for a direct cause-effect relationship between mineral and trace element status and atherosclerosis in humans, many elements exert a strong influence on individual risk factors for cardiovascular disease, such as disorders of blood lipids, blood pressure, coagulation, glucose tolerance, and circulating insulin. Studies in humans and animals have shown that optimal intakes of elements such as sodium, magnesium, calcium, chromium, copper, zinc, and iodine can reduce individual risk factors; some of these studies are consistent with the results of epidemiologic correlations. Influences of local geochemical environment and of dietary practices can result in mineral and trace element imbalances; deficiencies of chromium, iron, copper, zinc, selenium, and iodine are well defined. Detection and correction of such imbalances in populations, through diminishing individual risk factors, might ultimately reduce the incidence of atherosclerotic heart disease.
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PMID:Trace minerals and atherosclerosis. 674 52


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