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

Metabolic intermediate levels, glycolytic and Krebs cycle enzyme activities and lysosomal acid hydrolase activities were measured in aortas of spontaneously hypertensive (SHR) versus normotensive (WKY) rats. In the hypertensive aortas the level of lactate, the ratio of lactate to glucose and of lactate to malate was higher in the SHR than WKY aortas. In the hypertensive aortas the obvious shift of metabolism toward higher rate of glycolysis was associated with decreased activity of malate dehydrogenase and espically of lipoamide dehydrogenase. The latter is an essential compoenent of the alpha-ketoglutarate and pyruvate dehydrogenase enzyme complexes and it appears that these complexes are among the sites of arterialmetavolism which are primarily altered by the elevated blood pressure, resulting in increased production of lactate. The activity of the marker lysosomal enzyme N-acetyl-beta-glucosaminidase was unequivocally elevated in the hypertensive aortas. The activity of beta-glucuronidase exhibited incogruous differences between the SHR and WKY aortas and the activity of aortic acid phosphatase did not differ in the two rat strains. The results are discussed in relation to arterial injury, permeability, and atherogenesis.
Atherosclerosis 1977 Nov
PMID:Metabolic intermediates, enzymes and lysosomal activity in aortas of spontaneously hypertensive rats. 59 42

The locus for apolipoprotein-B (APOB) has been chromosomally assigned in swine by in situ hybridization of a genomic probe to metaphase chromosomes. As expected based on the observation of extensive linkage conservation and based on the previous assignment of the malate dehydrogenase locus (MDH1) in swine, APOB maps to chromosome 3, specifically to region 3q24-qter. Variations at APOB may represent both in humans and in swine risk factors for hypercholesterolaemia and atherosclerosis. Evidence presented here that the human and porcine APOB occupy evolutionarily conserved chromosome regions provides a basis for using the pig as an animal model to study the APOB associated atherosclerosis risk.
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PMID:Assignment of the pig apolipoprotein B locus (APOB) to chromosome region 3q24-qter. 157 Aug 95

Fourteen male rabbits born at elevation 4000 ft (first experimental series) were transferred at age of 2 months to elevation 12470 ft and raised there for 18 weeks. Half of the animals remained on a commercial rabbit chow (group H) while the other half was on the same diet supplemented with cholesterol (group C). Eight male rabbits raised at sea level served as controls (group S). Intima-media homogenates from the thoracic aortas were assayed for lactate dehydrogenase (LDH), malate dehydrogenase (MDH), lipoamide dehydrogenase, pyruvate kinase (PK), phosphofructokinase (PFK) and the lysosomal hydrolases beta-glucuronidase and N-acetyl-beta-glucosaminidase (NAGA). Aortic lactate and glucose were also measured. Thirty-two male rabbits (second experimental series) were subdivided into 4 groups. Rabbits were fed a cholesterol-supplemented diet not only at high altitude (8 rabbits matching group C) but also 8 animals raised at sea level. The degree of atherosclerosis in the aortas of these 4 groups was assessed by measuring the aortic cholesterol contents. Plasma cholesterol was also determined. In the aortas of the rabbits of group H the activity of PK was significantly elevated, and the activity of the lysosomal hydrolases significantly decreased compared with aortas of group S rabbits. There was no difference in the other enzyme activities or in the aortic glucose and lactate content of these groups. Cholesterol feeding of the animals of group C resulted in a significantly increased activity of the lysosomal hydrolases as well as of LDH and PK. The lipid analyses (second experimental series) revealed a trend to a lower concentration of aortic cholesterol in the high altitude than in the sea level animals, both fed a cholesterol diet, in spite of the higher plasma cholesterol concentrations in the high altitude animals. The low aortic lysosomal hydrolase activities in the high altitude rabbits are in accord with their comparatively lower susceptibility to experimental atherosclerosis. This metabolic feature may be due to a lower degree of exposure of these aortas to injurious factors, such as infections or lower blood pressure. The elevated activity of PK without increased lactate content in group H animals seems to parallel the well-known general adaptation of the organism to high altitude hypoxia, and does not indicate a metabolic switch toward anaerobic glycolysis.
Atherosclerosis 1984 Aug
PMID:Aortic enzymes and lactate in high altitude-raised and cholesterol-fed rabbits. 623 25

Trans unsaturated fatty acids are formed during hydrogenation of edible oils and their consumption in the United States has increased with increasing utilization of margarines. The effect of elaidic acid and trielaidin on atherosclerosis in cholesterol-fed rabbits were studied many years ago by Weigensberg and McMillan, who found these fatty acids to be significantly more hypercholesterolemic but not more atherogenic. Jackson et al. have found that trans fatty acids are not inordinately atherogenic in swine. We have fed rabbits semipurified, cholesterol-free diets containing either 3.2 or 6.0% of trans fatty acid. The diets were slightly hyperlipidemic but no more atherogenic than the control diet. We measured the activities of five hepatic enzymes (glucose-6-phosphatase, fatty acid synthetase, malate dehydrogenase, beta-hydroxybutyrate dehydrogenase, and monoamine oxidase [EC 1.4.3.4]). The diets affected only the activity of monoamine oxidase, which was lower in the livers of rabbits fed 6.0% trans fatty acid. Vervet monkeys were fed the same diets either for 1 year or for 6 months and then returned to the control diet for 6 months. The dietary manipulations had no effect on serum or lipid levels or aortic sudanophilia. Trans fatty acid levels of the serum reflected dietary concentration. Six months after cessation of feeding of the trans fat the levels of trans fatty acids in serum were virtually normal. Trans fatty acids appear to exert a hypercholesterolemic effect but do not influence aortic atherosclerosis in rabbits or aortic sudanophilia in vervet monkeys.
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PMID:Trans fatty acid effects in experimental atherosclerosis. 681 29

To test the effects of trans unsaturated fatty acids (t-FA) on atherosclerosis, lipidemia and enzyme activities, rabbits were fed a semipurified, cholesterol-free diet containing 40% sucrose, 25% casein and 14% fat for 5 months. Two experimental diets provided either 6% (high) or 3.2% (low) t-FA. The control group was fed a fat of composition similar to the two experimental diets but free of t-FA. Serum cholesterol and triglycerides were elevated in the rabbits fed 6% t-FA. Liver glycerides were also elevated in this group. The fatty acids of plasma, erythrocytes, epididymal fat, liver microsomes and liver mitochondria reflected the dietary composition. Levels of aortic atherosclerosis were identical in the three groups. There were no significant differences in activity of five hepatic enzymes: glucose-6-phosphatase (microsomal), fatty acid synthetase (cytosolic), malate dehydrogenase, beta-hydroxybutyrate dehydrogenase and monoamine oxidase (mitochondrial).
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PMID:Influence of trans unsaturated fats on experimental atherosclerosis in rabbits. 683 52

Cultured smooth muscle cells from pig aortas were incubated with low density lipoproteins (LDL) and chloroquine for up to 5 days, as an in vitro model for lipid accumulation in atherosclerosis. Cells incubated with LDL alone had a normal morphology, except that some cells contained large lipid droplets. The activities of acid phosphatase, catalase and malate dehydrogenase were increased in homogenates prepared from these cells. Cells incubated with chloroquine alone developed large autophagic vacuoles. The activities of the three acid hydrolases, acid phosphatase, N-acetyl-beta-glucosaminidase and beta-glucuronidase, were decreased, as was the proteolytic activity of the cell homogenates at acid pH toward 125I-labelled LDL. There was, however, a transient increase in the activity of malate dehydrogenase. Chloroquine by itself was toxic to the cells, but LDL protected against this toxic effect. Cells incubated with LDL and chloroquine together developed both autophagic vacuoles and large lipid droplets. The cholesteryl ester content of the cells was increased many-fold and the non-esterified cholesterol content was increased to a lesser extent. The above four acid hydrolase activities were decreased, as was the activity of catalase, whereas the activities of lactate dehydrogenase and malate dehydrogenase were increased.
Atherosclerosis 1982 Sep
PMID:Lipid accumulation in arterial smooth muscle cells in culture. Morphological and biochemical changes caused by low density lipoproteins and chloroquine. 715 Mar 93

Study of the key mechanisms, metabolism regulators, showed that in the blood of patients with atherosclerosis the NAD/NAD . N ratio decreases by 59.8% and the NAD+ concentration by 44%, while the NAD . N content increases by 56.7%. In the nicotinamide adenine dinucleotide system there is a general tendency tomards accumulation:the concentration of NADP+ grows by 218.6% and that of NADP . N by 12.9%. A marked increase in the content of incompletely oxidized products is determined: lactic acid by 37.4%, alpha-glycerophosphate by 49.8%, dihydroxyacetone phosphate by 155%, oxaloacetate by 131% in the presence of lactate dehydrogenase and malate dehydrogenase activation. The detected changes are evidence of tissue energy debt in atherosclerosis, they reflect the character of metabolic acidosis formation and point to the presence of conditions for intensified liposynthesis.
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PMID:[Content of nicotinamide coenzymes, metabolites and the NAD-dependent dehydrogenase activity in the blood in arteriosclerosis]. 737 12

A homogeneous preparation of malate dehydrogenase was obtained from human myocardium, the enzyme structure-functional properties were studied. Alterations in structure characteristics of the enzyme, increase in its hydrophobic moiety, decrease of the enzyme activity were observed during impairments in atherosclerosis. The alterations of the enzyme properties appear to be involved in deterioration of energy metabolism as well as they are related to activation of liposynthesis in atherosclerosis.
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PMID:[Structure-activity features of malate dehydrogenase from human myocardium in atherosclerosis]. 827 32

The active oxygen induced and free radical mediated oxidation of biological molecules, membranes, and tissues has been suggested as a major cause of cancer, atherosclerosis, and aging. Damage of endothelial cells may lead to cardiovascular and cerebrovascular diseases. In the present study, the antioxidant effect of pycnogenol (procyanidins extracted from Pinus maritima) was investigated in vitro using vascular endothelial cells. Confluent monolayers of bovine pulmonary artery endothelial cells (PAEC) were preincubated with different concentrations of pycnogenol for 16 h, washed, and then exposed to an organic oxidant t-butyl hydroperoxide (tBHP) for 3 or 4 h. Cellular injury was assessed by measuring cell viability with methylthiazol tetrazolium (MTT) assay and by determining the release of intracellular lactate dehydrogenase (LDH). Lipid peroxidation products of PAEC were monitored as malondialdehyde (MDA) with a thiobarbituric acid fluorometric assay. Incubation of tBHP (75, 100, or 125 microM) with PAEC decreased cell viability, increased LDH release, and elevated MDH production. Preincubation of PAEC with pycnogenol (10-80 micrograms/mL) before tBHP exposure significantly increased cell viability, decreased LDH release, and reduced MDA production. These results demonstrate that pycnogenol can protect vascular endothelial cells from oxidant injury. The data thus suggest that pycnogenol may be useful for the prevention of disorders associated with oxidative damage.
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PMID:Pycnogenol protects vascular endothelial cells from t-butyl hydroperoxide induced oxidant injury. 860 22