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

Oxidative damage due to free radical production is increased in uraemic patients and has been suggested as a possible factor contributing to the anaemia of chronic renal failure (CRF) and the pathogenesis of atherosclerosis. Oxidative stress was assessed in 40 patients with CRF maintained by either haemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) and in 18 healthy controls. Lipid peroxidation (assessed as malondialdehyde, MDA), total glutathione (TG), antioxidant enzyme (glutathione reductase (GSHRx), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD)) activity and antioxidant associated trace metal (selenium, copper, zinc) levels were studied. Erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). The results indicate increased levels of oxidative stress and altered erythrocyte membrane fluidity in patients treated with CAPD compared with controls and patients treated with HD. Only minor changes were observed in patients treated with HD. Altered free radical activity, oxidative stress and altered erythrocyte membrane fluidity observed in patients with CRF may contribute to the increase in vascular disease in such patients and to the anaemia of CRF.
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PMID:Oxidative stress and erythrocyte membrane fluidity in patients undergoing regular dialysis. 755 72

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

Methionine is converted by the transmethylation/transsulfuration pathway to homocysteine which may exert atherogenic effects by several mechanisms, including lipid peroxidation. Therefore, the excessive dietary methionine may induce the development of atherosclerosis. To test this hypothesis, plasma and aortic thiobarbituric acid reactive substances (TBARS), as well as activities of aortic and erythrocyte superoxide dismutase (SOD), catalase and selenium-dependent glutathione peroxidase (GPX) were measured in rabbits fed a diet enriched with 0.3% methionine for 6 or 9 months. Histological examinations of aortas also were performed. Feeding rabbits a methionine-enriched diet for 6 or 9 months resulted in significant increases in plasma and aortic TBARS levels and aortic antioxidant enzyme activities. However, a decrease in plasma antioxidant activity (AOA) was observed. In erythrocytes, SOD activity increased, catalase remained normal and GPX decreased in the treated animals. Histological examination of aortas showed typical atherosclerotic changes, such as intimal thickening, deposition of cholesterol, and calcification in methionine-fed rabbits. These results confirm that high-methionine diet may induce atherosclerosis in rabbits and indicate disturbances in lipid peroxidation and antioxidant processes as possible mechanisms of its atherogenic influence.
Atherosclerosis 1995 Jun
PMID:Increased lipid peroxidation as a mechanism of methionine-induced atherosclerosis in rabbits. 766 80

This review briefly summarizes the scientific evidence for a possible role of antioxidants in the prevention of coronary heart disease (CHD). Antioxidants in our diet include vitamins E, C, and beta-carotene, whereas selenium is an integral part of the antioxidant enzyme glutathione peroxidase (GSHPx). Experimental evidence suggests that free-radical damage and antioxidant defence may play an important role in the development of coronary heart disease. Epidemiological studies have produced some intriguing results, but have not indicated unequivocally that a high intake of antioxidants leads to a decreased cardiovascular disease risk. We conclude that the antioxidant atherosclerosis hypothesis is promising, but that the results of long-term intervention studies are still to be awaited. Preventive action based on antioxidant supplementation is therefore not justifiable as yet. Nevertheless, the findings so far certainly do support the recommendations for a varied diet rich in vegetables and fruit.
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PMID:Antioxidants and coronary heart disease. 769 69

The aim of this study was to examine whether physical and chemical working conditions explain the association of social class with ischaemic heart disease (IHD). We investigated the issue in a cohort of 2974 males aged 53-75 years (mean 63) free from overt cardiovascular disease. Potential confounders included were: alcohol consumption, physical activity, tobacco smoking, serum cotinine, serum lipids, serum selenium, body mass index, blood pressure, hypertension, social class, and retirement status. During the follow-up period (1985-1986 to 31 December 1991), 184 men (6.2%) had a first IHD event; 44 events were fatal. Compared to higher social classes (classes I, II and III), lower classes (classes IV and V) had a significantly increased risk of IHD (P < 0.05); the age-adjusted relative risk (RR) with 95% confidence limits was 1.44 (1.06-1.95), P = 0.02. Mean who had been occupationally long-term exposed (> or = 5 years) to either soldering fumes or organic solvents had a significantly higher risk of IHD than unexposed: RRs were 2.1 and 1.7, respectively. After adjustment for all the above potential confounders and including also these two occupational factors, the RR of low social classes was reduced to a non-significant 1.24 (0.87-1.76), P = 0.24, i.e. by 45%. Adjusting for non-occupational factors only reduced the RR from 1.44 to 1.38 (1.0-1.90), P = 0.05, i.e. by about 14%. Assuming that the association of soldering fumes and organic solvents with risk of IHD was causal, it was estimated that 16% of IHD cases in low social class could be ascribed to these exposures.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1995 Feb
PMID:Do physical and chemical working conditions explain the association of social class with ischaemic heart disease? 775 56

Patients with chronic renal failure, including those receiving regular long-term haemodialysis, have a high incidence of premature cardiovascular disease. Oxidative stress, which occurs when there is excessive free-radical production or low antioxidant levels, has recently been implicated as a causative factor in atherogenesis. The aim of this study was to determine if chronic renal failure and haemodialysis were associated with increased oxidative stress. Serum malondialdehyde was measured as a marker of lipid peroxidation in 15 patients with conservatively managed chronic renal failure (CRF), 15 patients with CRF undergoing regular haemodialysis and 15 healthy controls. Selenium, glutathione peroxidase and antioxidant vitamins were also measured. Malondialdehyde was elevated in dialysis patients in comparison to CRF and control groups (dialysis 1.16 +/- 0.08 mumol/l, CRF 0.94 +/- 0.07, controls 0.66 +/- 0.10). Antioxidants, including vitamin C, selenium and glutathione peroxidase, were decreased in dialysis patients and to a lesser extent in the CRF group (vitamin C-dialysis 16.43 +/- 3.76 mumol/l, CRF 34.5 +/- 8.6, controls 56.11 +/- 7.41; selenium-dialysis 0.77 +/- 0.07 mumol/l, CRF 0.69 +/- 0.06, controls 1.09 +/- 0.06: glutathione peroxidase-dialysis 101 +/- 5 U/l, CRF 160 +/- 11, controls 290 +/- 10). These findings indicate oxidative stress in patients with CRF which is further exacerbated by haemodialysis, as evidenced by increased lipid peroxidation and low antioxidant levels. This stress may play a role in the development of atherosclerosis in these groups.
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PMID:Oxidative stress in haemodialysis. 782 May 42

To obtain further insight into the role of selenium in the development of atherosclerosis, plasma selenium and lipid parameters were determined in 126 Portuguese subjects living in the region of Lisbon, 60 women and 66 men, 20-60 years old, divided up in to three groups according to their plasma lipid profile: Group I consisted of normolipidemic subjects having plasma triglycerides and total cholesterol < 200mg/dL; Group II was composed of hypercholesteremic subjects with total cholesterol > 200mg/dL and plasma triglycerides < 200mg/dL; Group III was composed of hypercholesteremic and hypertriglyceremic subjects having total cholesterol and plasma triglycerides > 200mg/dL. Respective values for mean plasma selenium (+/- SD) in the groups were: 93 +/- 18 micrograms/L, 90 +/- 17 micrograms/L and 96 +/- 18 micrograms/L. A weak significant difference in plasma selenium between women and men was, however, observed in Group I (87 +/- 20 micrograms/L vs. 100 +/- 11 micrograms/L, p < 0.05). Regression analysis showed no significant relationship between plasma selenium and lipid parameters, except in the most hyperlipidemic women of Group III, where a weak correlation between plasma selenium and the HDL-cholesterol/total cholesterol ratio (r = 0.80, p < 0.05) was observed. The present study suggests that the relationship between selenium and HDL-cholesterol has to be further examined, taking into account nutritional, metabolic and genetic factors.
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PMID:Selenium and lipid parameters in plasma of Portuguese subjects. 788 Dec 77

Selenium (Se) is an essential component of glutathione peroxidase (GSH-Px), an enzyme that protects cells by reducing intracellular peroxides. Impaired Se status and GSH-Px activity seem associated with increased risk of atherosclerotic vascular diseases. This study reports the effects of Se supplementation on GSH-Px activity, on prostacyclin (PGI2) production, on 12-hydroxy-eicosatetraenoic acid (12-HETE) levels, and on GSH-Px mRNA expression in cultured human umbilical vein endothelial cells (HUVEC). Se-enriched HUVEC showed significant increase of both GSH-Px activity and thrombin-stimulated production of PGI2 in the presence of stable concentrations of 12-HETE. On the other hand, an inverse correlation between Se concentrations in culture media and GSH-Px mRNA levels in Northern blot analysis was shown; this suggests that a major degree of regulation for GSH-Px expression by Se is most likely exerted at the posttranscriptional level. These observations may help to explain the increased incidence of atherosclerosis described in Se-deficient individuals.
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PMID:Selenium enhances glutathione peroxidase activity and prostacyclin release in cultured human endothelial cells. Concurrent effects on mRNA levels. 788 76

61 spa patients, predominantly with heart and vascular diseases, were divided into 2 therapeutic groups. In addition to the usual balneotherapeutic program, one group (J) received a course of "iodine brine concentrate" for drinking (2 x 100 ml, daily iodine uptake approximately 9 mg), and the control group (CI) received isotonic NaCl in the same way. The patients were mostly on a reduced-fat and -calorie diet. The following parameters were determined at the beginning and at the end of the 26-day treatment period: total cholesterol, HDL-cholesterol, triglycerides, lipoprotein (a) (in serum); selenium (Se), malondialdehyde (MDA), and activities of Se-dependent, Se-independent, and total glutathione peroxidase (GSH-PX) (in plasma). In the J group, a significant increase was found in Se-independent (+17%) and total GSH-PX (+5%) and a significant decrease in total cholesterol (-6.9%) and MDA (-13.2%). At the end of the cure, Se levels were higher in the J group than in the C1 group. The only significant change in the C1 group was a decrease in HDL-cholesterol. Positive correlations were found between selenium and Se-dependent GSH-PX (r = 0.253) and between total GSH-PX and Se-dependent GSH-PX (r = 0.665). A negative correlation was obtained between Se-dependent and Se-independent GSH-PX (r = -0.331). The results are discussed with regard to the importance of antioxidant defense mechanisms in several degenerative diseases (atherosclerosis, diabetes, cataract etc.), and also respecting interactions between iodine and selenium metabolism, as well as normalization effects conditioned by the balneotherapy itself.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in selenium status, antioxidant enzyme activity and lipid peroxide level after drinking cures in Bad Hall health resort]. 814 96

Abnormal regulation of local vascular tone occurs early in human and experimental atherosclerosis. Impaired endothelium-dependent vascular relaxations mediated by endothelium-derived relaxing factor are an important contributor to these abnormalities. Endothelium-derived relaxing factor is nitric oxide released as such or attached to a carrier molecule. Oxidized lipoproteins impede endothelium-derived relaxing factor-mediated responses in vitro. We designed in vivo experiments to determine whether hypercholesterolemia with and without deficiency of two endogenous lipid antioxidants, vitamin E and selenium, would result in endothelial dysfunction. Vitamin E and selenium deficiencies were induced in a group of hypertension-prone Dahl salt-sensitive rats fed a diet high in cholesterol (4%) but low in NaCl (0.5%) for 18 weeks. Two other groups of Dahl salt-sensitive rats received diets sufficient in vitamin E and selenium but containing either high or normal cholesterol levels (control group). Serum cholesterol levels increased approximately 10-fold in the two groups of rats fed high-cholesterol diets. Systolic blood pressure was 143 +/- 3 mm Hg in high-cholesterol/vitamin E- and selenium-sufficient rats and 142 +/- 5 mm Hg in high-cholesterol/vitamin E- and selenium-deficient rats (P = NS). Mild intimal thickening and occasional mononuclear cell infiltration were observed in both of these groups. Serum vitamin E levels were decreased, whereas serum thiobarbituric acid-reactive substances and exhaled pentane (two indicators of endogenous lipid oxidation) were significantly increased in high-cholesterol/vitamin E- and selenium-deficient rats compared with high-cholesterol/vitamin E- and selenium-sufficient rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercholesterolemia promotes endothelial dysfunction in vitamin E- and selenium-deficient rats. 831 92


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