Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum copper concentration increases significantly (p < 0.01) in rats with experimental atherosclerosis compared to a control group. The serum zinc, the zinc, and copper concentration in abdominal aorta and in liver decreases significantly (p < 0.05) compared to the control group. Administration of copper sulfate for 100 d in these animals induces a significant increase of serum copper (p < 0.01), decrease of serum cholesterol (p < 0.05) and increase of liver copper concentration as compared with the group fed only a high cholesterol diet. In the aorta of these animals the copper concentration increases and edema and lipid infiltration are considerably less than in the group of animals fed only a high lipid diet.
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PMID:Effect of copper sulfate on experimental atherosclerosis. 769 Nov 31

Zinc (Zn), an essential trace element, has antioxidant functions, stabilizes membranes, and plays a role in the activity of a host of Zn metalloenzymes. Zn deficiency has been shown to increase erythrocyte fragility, decrease the Zn content of the erythrocyte membrane, and alter erythrocyte membrane fluidity. Recent studies have shown that Zn deficiency induced by various mechanisms disrupts endothelial barrier cell function in vitro, and this was corrected with Zn supplementation. Moreover, physiological amounts of Zn attenuated the barrier dysfunction produced by the inflammatory cytokine tumor necrosis factor. These data have important implications for acute vascular processes, e.g., adult respiratory distress syndrome, and chronic vascular processes, e.g., atherosclerosis. The mechanisms by which Zn may affect endothelial cell function and attenuate cytokine-induced endothelial cell dysfunction are important areas of continuing investigation.
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PMID:Zinc and endothelial function. 774 57

The mechanism by which hyperinsulinemia promotes atherogenesis is unknown. The effects of hyperinsulinemia on risk factors for atherosclerosis were investigated by subcutaneously injecting rats daily with an insulin-zinc suspension (20 U/kg) for 12 weeks. After this period, body mass and food consumption did not differ significantly between control and insulin-treated animals. Daily insulin injection significantly increased urinary excretion of epinephrine and decreased urinary excretion of norepinephrine and dopamine, but had no significant effect on blood pressure or heart rate. Although insulin decreased plasma triglyceride concentration by 44% (P < .01), the triglyceride to protein ratio in plasma low-density lipoprotein (LDL) was increased by 34% (P < .05) in insulin-treated rats; the cholesterol to protein and triglyceride to protein ratios remained unaffected, indicating a change in the quality of the LDL particle. Insulin also increased the percentage of arachidonic acid (20:4) in LDL triglycerides by 37% (P < .05). In contrast, cholesteryl esters and triglycerides in the thoracic aorta were significantly increased (49% and 91%, respectively) by insulin treatment. Insulin increased the percentage of monounsaturated fatty acids and decreased the percentage of n-6 fatty acids, including arachidonate, in aortic triglycerides. Insulin also increased the percentage of palmitoleic acid (16:1) and decreased the percentages of saturated fatty acids and n-6 fatty acids in aortic cholesteryl esters. These results indicate that insulin induced deposition of cholesteryl esters and triglycerides, especially those containing monounsaturated fatty acids, and abnormal arachidonate distribution in LDL and tissues. The data further suggest that the development of atherosclerosis in response to hyperinsulinemia may be associated with arachidonate-rich triglycerides in LDL.
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PMID:Abnormal arachidonate distribution in low-density lipoprotein and thoracic aorta in hyperinsulinemia. 778 68

The relationship between zinc and atherosclerosis is reviewed. Administration of strong doses of the mineral can turn out atherogenic through three mechanisms: 1. Through the alterations of the lipidic arrangement: decrease of HDL, increase of total cholesterol and LDL cholesterol (action promoted by the induced hypocupremia). 2. Through the alterations of the vasal wall, in consequence of the biochemical modifications of the basic substance (again, through secondary hypocupremia). 3. Through the increased platelet aggregation which seems to be produced by strong doses of zinc. In addition to these harmful actions, the antioxidative action, typical of zinc, must be stressed, which prevents oxidation of LDL and consequently stops the main mechanism of atherogenesis. Besides, the mineral restricts and nullifies the loss of metallothionein in zinc, produced by free radicals and subsequent functional alterations. Moreover, the calcium antagonist action of zinc must be considered: it blocks calcium and its several favorable actions on atherogenesis. In consideration of these last aspects, the rule of zinc, in suitable doses, could be considered as basic in the context of a strategy of prophylaxis and therapy of the atherosclerosis process.
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PMID:[Zinc and atherosclerosis]. 785 58

The Cu, Zn, Cr, Fe, and Ni concentrations from the atherosclerotic plaques in the abdominal aorta obtained from 40 patients who died of coronary heart disease (CHD) were measured. In 32 of them the clinical and anatomical diagnosis was ischemic heart disease (IHD) and in 8 of them it was acute myocardial infarction (AMI). Concomitant determinations of the concentrations of the above trace elements were determined in 16 normal aortas from subjects who died in accidents or from causes other than atherosclerosis (C). The determinations were done by means of a Perkin-Elmer atomic absorption spectrophotometer, Model 300. The results are expressed in mg/kg of dried tissue. The Cu, Zn, and Cr concentrations were significantly lower (p < 0.01) in the atherosclerotic plaques of abdominal aorta of the deceased patients with IHD and AMI than in the control group. Iron had the tendency to rise but not significantly. The nickel level in the atherosclerotic plaques from abdominal aorta did not change significantly as compared to the controls. We attribute the low values of copper in the atherosclerotic aortic tissue in IHD and AMI to a shift of copper from aortic tissue into the blood. At present, there is no explanation for the low concentration of zinc and chromium in atherosclerotic aortic tissue.
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PMID:Concentration of copper, zinc, chromium, iron and nickel in the abdominal aorta of patients deceased with coronary heart disease. 788 Dec 75

Alteration of glycosaminoglycans (GAGs) in cultured bovine aortic smooth muscle cells after exposure to cadmium was investigated. It was revealed that cadmium increased the accumulation of GAGs metabolically labeled with [3H]glucosamine but decreased that with [35S]sulfate in the cell fraction, the cell surface fraction and the medium fraction. This suggested that cadmium stimulated the biosynthesis of GAGs but inhibited their sulfation in the cells. A similar alteration was observed in cadmium-treated human aortic smooth muscle cell layer. Of tested cations including cadmium, bismuth, cobalt, copper, lead, manganese, nickel and zinc, only cadmium stimulated [3H]glucosamine incorporation, with a strong inhibition of the [35S]sulfate incorporation in the bovine cells. Characterization of bovine smooth muscle GAGs showed that the cadmium-induced increase in the [3H]glucosamine incorporation was mainly observed in heparan sulfate; the inhibition of the [35S]sulfate incorporation occurred non-selectively. Cadmium accumulated in bovine vascular smooth muscle cells in a dose-dependent manner with an increase in the leakage of lactate dehydrogenase into the medium. The present data suggest that vascular smooth muscle cells respond to the cytotoxicity of cadmium and promote the GAG synthesis with a reduction of their sulfation. It is postulated that this response may be a defensive one to the damage of the vascular tissue caused by cadmium but would be a component of the metal-induced atherosclerosis.
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PMID:Alteration of glycosaminoglycans induced by cadmium in cultured vascular smooth muscle cells. 799 22

We have examined the effect of zinc ions on low density lipoprotein (LDL) oxidation by macrophages, endothelial cells and iron ions in terms of the increased uptake of the LDL by macrophages. Zinc ions inhibited LDL modification by both cell types (which is dependent on the presence of iron ions in the culture medium) and by iron ions alone. As oxidised LDL is believed to be involved in atherogenesis, this raises the possibility that zinc may be an endogenous protective factor against atherosclerosis.
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PMID:The oxidation of low density lipoprotein by cells or iron is inhibited by zinc. 813 49

The concentrations of calcium, magnesium, zinc, copper, free fatty acids and total, HDL- and LDL-cholesterol in the sera of atherosclerotic men were determined. The subjects with femoral atherosclerosis were divided into two age groups: 35-59 years (N = 8, I) and 60-75 years (N = 8, II). The LDL-cholesterol concentration was increased in the elderly atherosclerotic group. Lower concentrations of calcium and magnesium, a higher concentration of copper and decreased Ca/Cu, Mg/Zn, Mg/Cu and Zn/Cu ratios were found in atherosclerosis I as compared to controls of the same age. High and positive correlations for Cu vs. total cholesterol and LDL-cholesterol (r > 0.89), but low correlation for Cu vs. HDL-cholesterol (r = 0.61) were calculated in atherosclerosis I, and negative correlations for free fatty acids vs. Ca and Mg (-r > 0.77) in atherosclerosis II.
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PMID:Concentrations of calcium, magnesium, zinc and copper in relation to free fatty acids and cholesterol in serum of atherosclerotic men. 815 92

The frequencies of 10 diseases in a cadmium (and zinc) contaminated region in The Netherlands were analysed by comparing hospital admissions with those of a non-contaminated region and with national values. No significant differences were found for diseases which are commonly associated with increased cadmium uptake such as renal insufficiency, nephrolithiasis, hypertension, cancer, immaturity of the new-born. For the contaminated region a significantly higher frequency was only found for atherosclerosis; this was relatively strong for men aged > 40 yrs. However, no higher death frequency for atherosclerosis was observed. The results are discussed in relation to limitations in the evaluation techniques used. The absence of major health risks in the contaminated area is obvious, but the possible influence of long term-low level cadmium uptake on atherosclerosis requires more attention.
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PMID:Prolonged low-level cadmium intake and atherosclerosis. 825 93

Zn(II)-Phthalocyanine (Zn-Pc) is an exogenously administrable dye which is accumulated by tumors and other rapidly proliferating tissues. This property could be used for visualising atherosclerotic plaques. In order to define the feasibility and the optimal conditions for in vivo labelling of atheroma, we evaluated the ability of Zn-PC to be accumulated by experimentally induced atherosclerotic lesions in rabbits. We also performed pharmacokinetic investigations to assess photosensitizer delivery system, difference in phthalocyanine concentration between normal and atherosclerotic vessels, and the time interval after administration, which yields a large difference between normal and diseased vessels. We observed a preferential accumulation of Zn-Pc by atherosclerotic lesions which accumulated about a tenfold larger amount of photosensitizer, and the retention of significant amounts for prolonged periods. Zn-Pc can be considered as a potentially useful fluorescence marker for atheroma. The feasibility of photodiagnosis and phototherapy of atheroma deserves further investigation.
Atherosclerosis 1993 May
PMID:Targeting of experimentally induced atherosclerotic lesions by liposome-delivered Zn(II)-phthalocyanine. 835 53


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