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

Reticuloendothelial (RE) phagocytes (macrophages and histiocytes) can be distinguished from locally-derived lipid-containing cells (e.g., arterial smooth muscle) or locally derived phagocytes (e.g., Schwann cells and microglia) by the demonstration of a diffuse catalase reaction in a proportion of these RE cells with a short incubation modification of the Novikoff-Golfischer diaminobenzidine histochemical methods. Even though only a proportion of an RE population is catalase-positive, the results accord with the majority of current opinion that most of the cells in atherosclerotic lesions are derived locally, whereas the phagocytes in lipid implants and xanthomas are of RE origin. The phagocytes in the peripheral nerve undergoing Wallerian degeneration appear to be of mixed RE and endogenous origin, whereas microglia around multiple sclerosis plaques seem to be derived locally. Lipid in lesions with RE phagocytes (subcutaneous lipid implants and xanthomas) is relatively rapidly resorbed, whereas lipid in lesions with few RE phagocytes (atherosclerosis) or phagocytes of endogenous origin (CNS degeneration) is more slowly resorbed or partly retained within the tissue. Wallerian degeneration in the peripheral nerve, with its mixed population of RE and endogenous phagocytes, occupies an intermediate position in the speed of lipid removal.
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PMID:Phagocytes, lipid-removal and regression of atheroma. 81 81

Low density lipoprotein (LDL) oxidation mediated by phorbol myristate acetate (PMA)- and formylmethionylleucylphenylalanine (FMLP) -stimulated human neutrophils was enhanced by 70% in the presence of ferritin. Iron released from ferritin by the superoxide anion generated in the respiratory burst of stimulated neutrophils is shown to be involved in lipoprotein oxidation. Ascorbate (100 microM), superoxide dismutase (10 micrograms/ml) and uric acid (430 microM) showed inhibitory effects of 30% [corrected], 70% and 50% on LDL oxidation, respectively. Ceruloplasmin (2.7 microM) potentiated LDL oxidation by stimulated neutrophils and ferritin, both alone and in the presence of methionine. Methionine (1 mM) and catalase (30 micrograms/ml) increased LDL oxidation by stimulated neutrophils and ferritin. These data suggest that LDL oxidation by stimulated neutrophils and ferritin may be relevant in inflammation when both neutrophils and ferritin are increased.
Atherosclerosis 1992 Dec
PMID:Low density lipoprotein oxidation by stimulated neutrophils and ferritin. 133 54

Plasma lipid peroxidation, activity of erythrocyte superoxide dismutase (SOD) and catalase, and serum antioxidant activity (AOA) in uremic patients were examined before and after hemodialysis. An increased level of lipid peroxidation, a decreased serum AOA level, and elevated SOD and normal catalase activity before hemodialysis were observed in uremic patients compared with controls. Hemodialysis was found to produce increased lipid peroxidation, a simultaneous decrease of SOD activity, and lack of any changes in serum AOA and erythrocyte catalase. It is suggested that intensification of lipid peroxidation during hemodialysis could account for accelerated progress of atherosclerosis in patients with renal insufficiency.
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PMID:Effect of hemodialysis on lipid peroxidation and antioxidant system in patients with chronic renal failure. 143 96

To elucidate the role of oxygen free radicals and lipid peroxidation in the pathogenesis of early hypertension and atherosclerosis, we studied the native distribution of three primary arterial antioxidant enzymes (AEs). Specific immunohistochemical localization of superoxide dismutase (Cu-Zn SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) was examined in the arterial wall of New Zealand White rabbits: six sham-operated normotensive/normolipidemics (NT/NL), seven coarctation-induced hypertensive/normolipidemics (HT/NL), eight normotensive diet-induced hyperlipidemics (NT/HL), and six hypertensive/hyperlipidemics (HT/HL). All three AEs were confined primarily to the endothelium in NT/NL rabbit aortas. However, in HT and HL rabbits a greater proportion of the arterial wall, including the endothelium, inner media, and middle media, displayed immunolocalization of three AEs. Multiple linear-regression analysis revealed that more than 70% of the total variability in the depth of immunolocalization of arterial AEs could be explained by changes in blood pressure and/or total cholesterol. Also, levels of plasma and arterial cholesterol oxides were significantly different (p less than 0.05) in HT and HL rabbits compared with controls, with twofold increases in NT/HLs, threefold increases in HT/NLs, and fourfold increases in HT/HLs. We conclude that intense free-radical activity in the arterial wall of HT and HL animals is one possibility and that this occurs despite the presence of abundant AEs.
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PMID:Immunolocalization of native antioxidant scavenger enzymes in early hypertensive and atherosclerotic arteries. Role of oxygen free radicals. 155 32

Lipid peroxidation and the antioxidant status were studied in male patients having stable angina (SA) and unstable angina (UA) pectoris and the results were compared with that of controls. Lipid peroxides (LPx) and conjugated dienes (CD) were found to be elevated in patients with both SA (LPx: 3.96 +/- 1.07, P less than 0.001; CD: 357.09 +/- 66.23, P less than 0.01) and UA (LPx: 4.66 +/- 1.33, CD: 373.33 +/- 49.82, P less than 0.001) than in controls (LPx: 3.22 +/- 0.86, CD: 335.15 +/- 60.27). In SA, the erythrocytes expressed a diminished activity of superoxide dismutase (SOD) (SA: 435.59 +/- 76.02, control: 651.69 +/- 145.90, P less than 0.001) and normal activities of catalase and glutathione peroxidase, whereas in UA it showed enhanced activities of both SOD (UA: 735.72 +/- 145.67, P less than 0.01) and catalase (UA: 21.94 +/- 6.26, control: 18.69 +/- 6.37, P less than 0.01). A significant increase was also noticed in the levels of ceruloplasmin and vitamin E during both types of angina, but not alteration was observed in the levels of transferrin. Further, the patients with diabetes showed maximum levels of lipid peroxides compared to smokers and hypertensives. The level of lipid peroxides was also observed to increase with the severity of disease. This study indicates that free radicals are involved in the pathogenesis and progression of atherosclerotic heart disease.
Atherosclerosis 1992 Jun
PMID:Antioxidant status in relation to free radical production during stable and unstable anginal syndromes. 163 72

We performed an in vitro study to assess damage to swine aortic endothelial cells by rabbit beta-VLDL and/or rabbit peritoneal macrophages. Incubation of cultured aortic endothelial cells with beta-VLDL, macrophages, or macrophage lysate induced endothelial cell damage time- and dose-dependently as estimated by [3H]adenine release. Incubation of endothelial cells with both beta-VLDL and macrophages produced a synergistic effect on the increase of [3H]adenine release. Pretreatment of the endothelial cells with some kinds of antioxidants (probucol 50 micrograms/ml, vitamin E 50 microM, superoxide dismutase-polyethylene glycol 0.5 mg/ml, or catalase-polyethylene glycol 0.5-1.0 mg/ml) significantly prevented the endothelial damage by beta-VLDL or macrophage lysate. We conclude that beta-VLDL and/or macrophages could induce endothelial cell damage and that some kinds of antioxidants could prevent it.
Atherosclerosis 1990 Dec
PMID:Aortic endothelial cell damage induced by beta-VLDL and macrophages in vitro. 210 79

A segment of fresh rabbit thoracic aorta (RbA) was turned inside out and superfused (1.5 ml/min) with citrated (3.8%) or heparinized (10 U/ml) blood of rabbit and the superfusate was discarded. RbA gained in weight due to deposition of thrombi on its endothelial surface. These thrombi were mainly composed of platelets. The interaction between platelets and endothelium was augmented in RbAs from animals with atherosclerosis and in RbAs pretreated with aspirin (110 microM) or 15-HPETE (150 microM) or by the enzymatic system generating oxygen free radicals (xanthine:xanthine oxidase - 100 microM: 0.1 U/ml). On the other hand, this interaction was impaired by superoxide dismutase (20 U/ml) or catalase (0.2 U/ml). Finally, the dissipation of thrombi by thromboxane A2-synthetase inhibitor--dazoxiben was found to be related to an increase in endothelial generation of prostacyclin.
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PMID:A biological method for studying the interaction between platelets and vascular endothelium. 210 94

Oxygen reactive species are normally formed in cells and play an essential part of the bactericidal activity of phagocytic cells. The damaging effect of these oxygen reactive species is prevented by the endogenous scavengers SOD, glutathione peroxidase, catalase, circulating transferrin, ascorbic acid, and membrane-bound alpha-tocopherol. However, when excess amounts of oxygen radicals and hydrogen peroxide are formed, as in reperfusion injury or trauma, the endogenous scavengers are insufficient to react with these active molecules. Lipid peroxidation is an important part of the formation of oxygen reactive species. Lipid peroxidation, especially peroxidation of LDL, may have a significant role in atherosclerosis. Thus dietary manipulation of PG and TX formation through either feeding cold water fish oils or plant oils containing high amounts of polyunsaturated fatty acids may be a two-edged sword. Also, the dietary manipulation of arachidonic acid through increasing its precursor linoleate may cause a decrease in the immune response as seen in animal experiments. The marine oils may be regarded as a natural aspirin in that formation of PGs of the bisenoic series will be replaced by the PGs of the trienoic series. This results in the formation of TXA3, which is biologically inactive, and PGI3, which is biologically active like PGI2. This may have no physiologic consequences but it is used to illustrate a possible mechanism for the postulated beneficial cardiovascular effects of these oils. The issues and the mechanisms are controversial and frequently highly speculative. The subject is a boon for the lipid biochemist and nutritionist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radicals, arachidonic acid metabolites, and nutrition. 212 35

Adult male New Zealand white rabbits were fed for 3 months a stock diet supplemented with 6% (w/w) soybean oil heated at 240 degrees C for 60 min. After the first month of treatment a significant increase in total lipid content of serum was observed mainly due to the cholesterol ester fraction. Simultaneously, grossly induced atherosclerosis and marked liver damage were histologically and clinically demonstrated. Lipid peroxide values, performed by thiobarbituric acid test in lipid extracts from liver, aorta and bile showed a significant increase as compared to controls. Lipoperoxidation rate increased with the duration of feeding. Parallel to this there was a marked reduction in the activities of glutathione peroxidase, superoxide dismutase and catalase in liver and aorta, all enzymes involved in the mechanism of detoxification of lipid peroxides. The results are in agreement with the hypothesis that lipid peroxidation can play a significant role in the pathogenesis of atherosclerosis.
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PMID:Serum and biliary lipid pattern in rabbits feeding a diet enriched with unsaturated fatty acids. 227 34

In 24 rabbits fed a hyperlipidic diet (0.5% cholesterol, 5% lard and 5% peanut oil) for 10 (group A1), 30 group B1) and 60 days, (Group C1), compared to 24 control rabbits fed a standard diet for the same periods, antioxidant defence system (total superoxide dismutase, catalase, total thiol compounds selenium-dependent and selenium-independent glutathione peroxidase, glutathione reductase, glutathione transferase) and lipid peroxidation (thiobarbituric acid-reactive substances) in the aortic wall were tested. The percent of intima with grossly apparent atherosclerosis, is assessed by staining with the lipophilic dye Sudan IV, was negligible in group A1, but increased progressively in groups B1 (22.7-6.7%) and C1 (56.8-8.8%). Compared to the controls, a significant rise in superoxide dismutase activity was observed after 30 days of hyperlipidic diet, with a further marked increase at 60 days. Total thiol compounds and selenium-dependent glutathione peroxidase activity rose progressively from 10 to 30 and 60 days in cholesterol-fed rabbits. On the contrary, catalase, glutathione reductase and glutathione transferase activities significantly decreased in all experimental groups. Selenium-independent glutathione peroxidase activity was not detectable. Thiobarbituric acid-reactive substances increased about 3 times in hyperlipidemic rabbits. In conclusion, the changes in aortic antioxidant defence mechanisms and lipid peroxidation precede the massive vascular lipid infiltration in cholesterol-fed rabbits; some antioxidant mechanisms are stressed (superoxide, dismutase, glutathione peroxidase, total thiol compounds), whereas others are depressed (catalase, glutathione reductase, and glutathione transferase), thus potentially reducing or increasing vascular susceptibility to oxidative injury.
Atherosclerosis 1990 Mar
PMID:Aortic antioxidant defence mechanisms: time-related changes in cholesterol-fed rabbits. 232 23


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