UMLS:C0004153 - FACTA Search

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

In the paper the authors synthetically discuss the aetiology and pathogenesis and point to the possibilities of prevention of one of the most important groups of diseases developing as the result of faulty nutrition--circulatory system diseases. In the first part the epidemiology is discussed of the system's diseases--ischaemic heart disease, hypertension, cerebrovascular diseases--stressing the extent of the health problem caused by them--over 50% of deaths each year are due to these diseases. Then, the main cause is discussed of the development of cardiovascular system diseases, that is atherosclerosis. The risk factors are characterized in which nutrition plays an essential role - blood level of cholesterol, its content in low (LDL) and high (HDL) density lipoproteins, triglyceride level, content of saturated fatty acids in diet. Nutritional preventive factors are briefly described--mono- and polyunsaturated fatty acids, vitamin E, cellulose. The beneficial effect of increased fish consumption is stressed. The last part deals with arterial hypertension as the disease of the vascular system and as the risk factor of ischaemic heart disease. The attention is paid to the necessity of changes in nutrition mode--increase of the supply of mono- and polyunsaturated fatty acids with predominance of the former, decrease of the supply of saturated fatty acids, salt, ensuring of adequate supply of antioxidant vitamins and cellulose. In the paper it is stressed that the modern state of knowledge, used in practice may significantly decrease in Poland, through nutrition, the epidemic of circulatory system diseases similarly as it has been done in other countries.
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PMID:[The role of nutrition in the development of circulatory system diseases]. 748 27

Persons with diabetes are at increased risk for developing coronary heart disease (CHD): although the standard risk factors are also applicable, there are other major nontraditional risk factors for these persons. For example, oxidation of lipoproteins may play an important role in the development of atherosclerosis. Another risk factor is the presence of small, dense low-density lipoprotein (LDL), which may have enhanced atherogenicity because it enters the arterial wall more readily and is more easily oxidized. Both of these factors may be particularly important in persons with non-insulin-dependent diabetes mellitus (NIDDM), because these persons may have greater rates of lipid oxidation in vivo than do nondiabetic persons and also have an increased prevalence of small, dense LDL. I describe potential dietary and pharmacologic regimens in patients with NIDDM to decrease in vivo lipid peroxidation, and the susceptibility of LDL and dense LDL subfractions to oxidative modification. In nearly all NIDDM patients, reducing dietary saturated fat helps lower plasma cholesterol and reduces the risk for CHD. There is, however, some controversy as to whether dietary saturated fat should be replaced by carbohydrates or by monounsaturated fatty acids (MUFAs) in NIDDM. Recent studies showed reduced susceptibility to oxidation of LDL in subjects consuming MUFA-enriched diets, thus adding another dimension to the ongoing debate over the most appropriate diet for NIDDM patients. Additionally, supplemental antioxidants such as probucol and vitamin E alone or in combination with MUFA-enriched diets have shown promise in protecting LDL from oxidation when given to nondiabetic populations. I also present recent results from an antioxidant trial in NIDDM subjects.
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PMID:Dietary and pharmacologic regimens to reduce lipid peroxidation in non-insulin-dependent diabetes mellitus. 749 49

A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro- and macrovascular endothelium. A previous study, using a skinfold chamber model for intravital fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro- and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 +/- 11.0 vs. 149.6 +/- 38.7 leukocytes per mm2, P < 0.01; arterioles, 8.5 +/- 4.2 vs. 54.3 +/- 21.6 leukocytes per mm2, P < 0.01; aortas, 0.8 +/- 0.4 vs. 12.4 +/- 5.6 leukocytes per mm2, P < 0.01; means +/- SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CS-induced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 +/- 22.2 microM, n = 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.
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PMID:Vitamin C prevents cigarette smoke-induced leukocyte aggregation and adhesion to endothelium in vivo. 751 84

Mounting evidence supports current theories linking lipoprotein oxidation to atherosclerosis. We sought the cellular biochemical mechanism by which oxidized LDL inflicts cell injury. Inhibitors of candidate pathways of cell death were used to treat human fibroblast target cells exposed to oxidized LDL.. Ebselen, which degrades lipid hydroperoxides, inhibited oxidized LDL toxicity, consistent with our recent report that 7 beta-hydroperoxycholesterol (7 beta-OOH chol) is the major cytotoxin of oxidized LDL. Intracellular chelation of metal ions inhibited, while preloading cells with iron enhanced, toxicity, Inhibition of oxidized LDL and 7 beta-OOH chol toxicity by 2-keto-4-thiolmethyl butyric acid, a putative alkoxyl radical scavenger and by vitamin E, probucol and diphenylphenylenediamine, putative scavengers of peroxyl radicals was consistent with the involvement of these radicals in the lethal sequence. Cell death was thus postulated to occur due to lipid peroxidation via a sequence involving lipid hydroperoxide-induced, iron-mediated formation of alkoxyl, lipid, and peroxyl radicals. Pathways involving other reactive oxygen species, new protein synthesis, or altered cholesterol metabolism were considered less likely, since putative inhibitors failed to lessen toxicity. Understanding the mechanism of cell injury by oxidized LDL and its toxic moiety, 7 beta-OOH chol, may indicate specific interventions in the cell injury believed to accompany vascular lesion development.
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PMID:In vitro cell injury by oxidized low density lipoprotein involves lipid hydroperoxide-induced formation of alkoxyl, lipid, and peroxyl radicals. 756 78

Oxidatively damaged LDL may be of central importance in atherogenesis. Epidemiological evidence suggests that high dietary intakes of beta-carotene and vitamin E decreases the risk for atherosclerotic vascular disease, raising the possibility that lipid-soluble antioxidants slow vascular disease by protecting LDL from oxidation. To test this hypothesis, we fed male New Zealand White rabbits a high-cholesterol diet or the same diet supplemented with either 1% probucol, 0.01% vitamin E, 0.01% all-trans beta-carotene, or 0.01% 9-cis beta-carotene; then we assessed both the susceptibility of LDL to oxidation ex vivo and the extent of aortic atherosclerosis. As in earlier studies, probucol protected LDL from oxidation and inhibited lesion formation. In contrast, vitamin E modestly inhibited LDL oxidation but did not prevent atherosclerosis. While beta-carotene had no effect on LDL oxidation ex vivo, the all-trans isomer inhibited lesion formation to the same degree as probucol. Moreover, all-trans beta-carotene was undetectable in LDL isolated from rabbits fed the compound, although tissue levels of retinyl palmitate were increased. The effect of all-trans beta-carotene on atherogenesis can thus be separated from the resistance of LDL to oxidation, indicating that other mechanisms may account for the ability of this compound to prevent vascular disease. Our results suggest that metabolites derived from all-trans beta-carotene inhibit atherosclerosis in hypercholesterolemic rabbits, possibly via stereospecific interactions with retinoic acid receptors in the artery wall.
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PMID:Beta-carotene inhibits atherosclerosis in hypercholesterolemic rabbits. 756 Jan 2

Peroxidation of low density lipoproteins (LDL) may be involved in the development of atherosclerosis which is prevalent in patients with chronic renal failure and renal transplant recipients. We determined the copper ion catalyzed oxidation in vitro, vitamin E content, and chemical and fatty acid composition of LDL isolated from 38 patients with renal disease and 15 healthy subjects. Also the acute effect of hemodialysis treatment on LDL oxidation variables was tested. The lag time in conjugated diene formation during oxidation was significantly (P = 0.011) shorter in LDL from renal transplant recipients (66 min, N = 18) mainly due to significantly (P < 0.05) shorter times in women (47 min, N = 7), compared with healthy subjects (83 min, N = 15), patients on hemodialysis (91 min, N = 13) and patients treated by continuous ambulatory peritoneal dialysis (CAPD) (82 min, N = 7). The maximum rate and the extent of LDL oxidation were significantly (P < 0.01) lower in all patients with renal disease compared with healthy subjects. The triglyceride content of LDL was significantly (P < 0.001) higher in women with kidney grafts (7.3%) compared with levels in the corresponding men (5.3%) and healthy women (5.0%), and was correlated significantly with the lag time in LDL oxidation in renal transplant recipients (Spearmans r = -0.502, P = 0.034). The percentage oleic acid in LDL was significantly higher (P = 0.002) and the percentage linoleic acid was significantly lower (P = 0.046) in patients with renal disease, and may largely account for their lower rates and extent of LDL oxidation. Levels of the LDL oxidation variables and organic lipid peroxide content of LDL were not significantly different before and after hemodialysis and 24 hours later. These results suggest that LDL from women with renal transplants may be abnormally susceptible to oxidation possibly due to increased triglyceride content.
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PMID:Oxidation of low density lipoproteins from patients with renal failure or renal transplants. 756 83

Vitamin E is a potent, naturally occurring, lipid-soluble antioxidant, which is reported to be protective against several disease processes, including coronary atherosclerosis. We have measured the alpha-tocopherol content of the aorta, liver, skeletal muscle, and kidney of rats fed one of the following diets for 10 weeks: a normal control chow diet (i); or the same diet containing 1% cholesterol (ii); 0.5% vitamin E (iii); or 1% cholesterol plus 0.5% vitamin E (iv). The alpha-tocopherol content of serum and tissue extracts was measured by HPLC using gamma-tocopherol as an internal standard. Tissue and serum cholesterol content was measured using a cholesterol oxidase enzyme reagent kit. In all animals receiving the 1% cholesterol diet, serum cholesterol levels increased significantly (P < 0.005). By the 10th week, mean serum alpha-tocopherol levels rose significantly in both groups of animals receiving dietary vitamin E supplements (P < 0.0001) compared with their respective control group. This was accompanied by a significant increase in the absolute alpha-tocopherol content of liver (8- to 9-fold) and aorta (3- to 4-fold). The alpha-tocopherol content of renal and skeletal muscle tissue was raised 1- to 2-fold in both groups of rats on vitamin E supplements, however the increased attained significance only for the renal tissue. The aortic tissue alpha-tocopherol/cholesterol ratio was 4-fold higher in the rats receiving concomitant 1% cholesterol plus 0.5% vitamin E compared with animals receiving 1% cholesterol alone (P < 0.02), and was 5-fold higher in the rats receiving 0.5% vitamin E compared with those receiving control chow (P < 0.01). These data suggest that dietary vitamin E supplementation results in a differential uptake of alpha-tocopherol, which may be dependent, in part, on selective lipoprotein particle accumulation.
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PMID:Tissue distribution of alpha-tocopherol following dietary supplementation in the rat: effects of concomitant cholesterol feeding. 756 86

The hypothesis that oxidative modification of low density lipoprotein contributes to the progression of atherosclerosis is supported by an impressive body of in-vitro findings and by persuasive results in animal models of atherosclerosis. The hypothesis was originally proposed specifically to account for foam cell formation but oxidation of LDL has now been shown to confer on it a long list of new biological properties any one of which could in principle enhance its atherogenicity. The relative importance of these altered biological properties in vivo remains uncertain. Whatever the precise mechanisms, we know that antioxidants can slow the atherogenic process in several experimental models, including LDL-receptor-deficient rabbits, cholesterol-fed rabbits, and cholesterol-fed non-human primates. Of 18 published studies, 13 have given strongly positive results, the rate of progression of lesions being reduced by 50-80%; 2 have yielded marginally positive results; and 3 have been negative (see ref 3 for references). Furthermore, the fact that four different antioxidant compounds have been used--probucol, butylated hydroxytoluene, N,N'-diphenyl-phenylenediamine, and vitamin E--supports the conclusion that they are working via the property they all share, namely, their antioxidant potential.
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PMID:Clinical trials of antioxidants in atherosclerosis: are we doing the right thing? 760 47

The effects of 3 days' exposure to native and oxidatively modified human low density lipoprotein (LDL and Ox-LDL) on cultured bovine aortic endothelial cell cholesterol content, membrane microviscosity and intracellular free calcium concentration ([Ca2+]i) were studied. Free cholesterol content increased by 35% and 100% in LDL and Ox-LDL treated cells, respectively, these effects being reversed by vitamin E; esterified cholesterol, which rose by 110% in the Ox-LDL group only, was not affected by vitamin E. Membrane microviscosity, measured as the fluorescence polarization of the trimethylammonium derivative of diphenyl-hexatriene, increased by 9% in Ox-LDL treated cells only. This effect was also reversed by vitamin E. Using the calcium sensitive fluorescent dye fura 2-AM, increases in basal [Ca2+]i of 36% in LDL and 81% in Ox-LDL treated cells were observed. The bradykinin mediated increase in [Ca2+]i was enhanced in both the LDL and, to a greater extent, the Ox-LDL group. Vitamin E reversed the effects of LDL on [Ca2+]i but had no influence in the Ox-LDL group. The lipoproteins affected all parameters measured in this study. Oxidized LDL produced reversible and irreversible alterations to the membrane and the [Ca2+]i. All changes associated with LDL were abolished by vitamin E. Such modifications in the physicochemical properties of the membrane and [Ca2+]i could be involved in the initiation of the atherosclerotic process.
Atherosclerosis 1995 Apr 24
PMID:Oxidized-LDL induced changes in membrane physico-chemical properties and [Ca2+]i of bovine aortic endothelial cells. Influence of vitamin E. 760 87

Evidence is accumulating that most of the degenerative diseases that afflict humanity have their origin in deleterious free radical reactions. These diseases include atherosclerosis, cancer, inflammatory joint disease, asthma, diabetes, senile dementia and degenerative eye disease. The process of biological ageing might also have a free radical basis. Most free radical damage to cells involves oxygen free radicals or, more generally, activated oxygen species (AOS) which include non-radical species such as singlet oxygen and hydrogen peroxide as well as free radicals. The AOS can damage genetic material, cause lipid peroxidation in cell membranes, and inactivate membrane-bound enzymes. Humans are well endowed with antioxidant defences against AOS; these antioxidants, or free radical scavengers, include ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), beta-carotene, coenzyme Q10, enzymes such as catalase and superoxide dismutase, and trace elements including selenium and zinc. The eye is an organ with intense AOS activity, and it requires high levels of antioxidants to protect its unsaturated fatty acids. The human species is not genetically adapted to survive past middle age, and it appears that antioxidant supplementation of our diet is needed to ensure a more healthy elderly population.
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PMID:The role of free radicals in disease. 761 52

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