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

Copper deficiency adversely affects the extracellular matrix of the arterial wall, leading to cardiovascular lesions. To study the lesions resulting from copper deficiency, the composition of proteoglycans from aortas of copper-deficient rats was compared with proteoglycans of aortas from copper-supplemented rats. Copper deficiency in rats was verified by copper levels in adrenal glands (mean +/- SE, 0.37 +/- 0.07 vs 1.03 +/- 0.17 micrograms/g wet wt in supplemented rats). The proteoglycans were isolated from the aorta by extraction with 4 M guanidine-HCl and by digestion of the tissue with elastase. The proteoglycans were purified by CsCl isopycnic centrifugation and fractionated by gel filtration. The fractions were characterized for molecular size and glycosaminoglycan composition. Total uronate in the aortas from copper-deficient rats was 25% greater than in aortas from copper-supplemented rats, and the proteoglycans from copper-deficient rat aortas were of greater molecular size. Among the glycosaminoglycans the concentration (microgram/mg tissue) of isomeric chondroitin sulfates, particularly dermatan sulfate, was greater in copper-deficient animals than in copper-supplemented animals. These observations are similar to earlier findings in experimental atherosclerosis and to a response of cardiovascular connective tissue to injury.
 ...
PMID:Composition of proteoglycans in the aortas of copper-deficient rats. 291 12

Copper deficiency has been shown to result in severe cardiovascular lesions in several species of animals. The principal carbohydrate in the copper-deficient diet most often used with rats is sucrose, which is known to have adverse effects on carbohydrate and lipid metabolism and thus may contribute to cardiovascular disorders. These observations prompted experiments in which starch and fructose were substituted for sucrose in a copper-deficient diet, to see if the effects of the copper deficiency might be modified. In the hearts from rats fed copper-deficient diets with fructose or sucrose, there was marked, mostly ventricular hypertrophy, and mild to severe myocardial inflammation, degeneration, and fibrosis. Aneurysm of the left ventricle and pericarditis also were common. Hearts from the starch, copper-deficient groups were much less hypertrophic, and very few were affected by myocardial inflammation, degeneration, or fibrosis. Defects of elastin or other structures were not observed in the aortas or pulmonary or coronary arteries of any specimens.
Atherosclerosis 1988 Dec
PMID:Dietary fructose exacerbates the cardiac abnormalities of copper deficiency in rats. 324 Mar 32

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.
 ...
PMID:[Zinc and atherosclerosis]. 785 58