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

ADVERSE EFFECTS OF OXYGEN: Adverse effect of oxygen on anaerobes implies oxidation of the basic cell constituents NAD(P)H, thiols, iron-sulphur proteins, pteridines and others) and inactivation of the essential components of the active site of enzymes. Oxygen can also adversely affect the aerobes, especially if long-term influence is taken into consideration, while exposition to high-pressure oxygen causes considerable damages. Direct influence of oxygen on aerobes due to slow and limited enzyme inactivation (for example glutamate decarboxylase) and small number of affected "targets" is not responsible for total adverse effects of oxygen. Even in 1954 it was supposed that oxygen free radicals are the most responsible for the adverse effects of oxygen. ATMOSPHERIC (TRIPLET) OXYGEN: Electron configuration of triplet oxygen explains its reactivity since it is a biradical. The reactions of oxygen with non-radicals are possible with participation of transition metals (except zinc), while its reactivity is much more expressed in case of reactions with other radical species. ACTIVE OXYGEN: More reactive forms of oxygen, known as singlet oxygen, can be generated by an input of energy to triplet oxygen. Singlet-oxygen is obtained mainly by photoexcitation in the presence of initiators (methylene blue, chlorophyll etc.) and as a product of reactions of ozone with certain biomolecules. REDUCED FORMS OF OXYGEN: If a single electron is added to the triplet oxygen, it must enter one of the antibonding molecular orbitals and produce the superoxide radical--(O2.-). Addition of one more electron produces peroxide ion--O2(2-), which forms hydro peroxide in presence of H+, the most common two-electron reduction product of oxygen in biological systems. The four-reduction product of oxygen in biological systems is water. SUPEROXIDE RADICAL: The in vivo production of superoxide radical is possible in many different ways mentioned in this paper. This radical species is unstable in water solutions because of dismutation reaction leading to non-enzymic generation of hydroperoxide. The most reactive radical species--hydroxyl radical is produced from hydro peroxide by Fenton or Haber-Weiss reactions in the presence of catalytic transition metals (iron or copper). HYDROXYL RADICAL: Hydroxyl radicals are the most reactive radical species. The way of their generation has been shown in detail in this paper with special emphasis given to Fenton and Haber-Weiss reactions, that is, transition metals (iron and copper) as catalizators for these reactions. The reactivity of hydroxyl radical can be recognized by monitoring the second-order rate constants for reactions of the hydroxyl radical with some organic compounds in aqueous solution presented in this paper. Although the number of compounds that can be affected and damaged by hydroxyl radicals is great, until now, attention has been paid mostly to investigation of attacks of these radical species on lipids, proteins and DNA. LIPID PEROXIDATION: Radicals react with lipids and cause oxidative destruction of unsaturated, that is, polyunsaturated fatty acids, known as lipid peroxidation. Both lipids in biological systems and lipids as food constituents are submitted to this process. Lipid peroxidation is a chain reaction and its mechanism has been shown in detail in this paper. Lipid peroxidation in cells leads to direct damage of cell membranes with indirect damages of other cell constituents, caused by reactivity of secondary products of this reaction, aldehydes. This complex reaction is responsible for damages of many tissues and progress of some diseases (atherosclerosis). OXIDATIVE STRESS: Protection of an organism from oxygen free radicals implies activity of enzymatic (catalase, SOD, glutathione peroxidase, glutathione reductase etc.) and nonenzymatic (vitamin E. vitamin C. glutathione, uric acid etc.) systems of protection. Disturbance of the balance between production of oxygen free radicals (or some other radical species) and activity of antioxidative system of protection causes the so called oxidative stress. An organism can tolerate a mild oxidative stress but a higher disturbance between the production of free radicals and the activity of the antioxidative protection results in lipid protein and DNA as well as numerous diseases.
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PMID:[Free oxygen radiacals and kidney diseases--part I]. 1132 Jul 27

The present study describes the effects of several high-fat low-cholesterol antiatherogenic diets on the hepatic lipid peroxidation and hepatic antioxidant systems in apolipoprotein E-deficient mice. Eighty mice were distributed into five groups and fed with regular mouse chow or chow supplemented with coconut, palm, olive and sunflower seed oils. After ten weeks, they were sacrificed and the livers were removed so that lipid peroxidation and alpha-tocopherol concentrations, and superoxide dismutase, glutathione peroxidase and glutathione reductase activities could be measured. The size of the atherosclerotic lesions in the aortas was also measured. Results showed that the diets supplemented with olive oil, palm oil or sunflower seed oil significantly decreased the size of the lesion. However, there was an association between those mice that were on diets supplemented with palm or coconut oils and a significant increase in hepatic lipid peroxidation. This association was not found in animals fed with olive or sunflower seed oils, the diets with the highest content of vitamin E. The dietary content of vitamin E was significantly correlated (r = 0.98; p < 0.05) with the hepatic concentration of this compound. Our study suggests that the high content of vitamin E in olive oil or sunflower seed oil may protect from the undesirable hepatotoxic effects of high-fat diets in apo E-deficient mice and that this should be taken into account when these diets are used to prevent atherosclerosis.
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PMID:Effects of high-fat, low-cholesterol diets on hepatic lipid peroxidation and antioxidants in apolipoprotein E-deficient mice. 1133 Aug 32

Damage to the vascular endothelium by reactive oxygen species causes many cardiovascular diseases including atherosclerosis. Such damage can be prevented by selenium (Se), which is thought to exert its actions mainly through the expression of selenoproteins. Se deficiency increased the susceptibility to tert-butylhydroperoxide (t-BuOOH) and enhanced lipid peroxidation in bovine arterial endothelial cells (BAEC). We investigated the effects of Se deficiency on the expression of the selenoproteins in BAEC. 75Se metabolic labeling analysis and RT-PCR analysis revealed that BAEC expressed two glutathione peroxidase (GPx) isozymes, cytosolic GPx (cGPx) and phospholipid hydroperoxide GPx (PHGPx), three thioredoxin reductase (TrxR) isozymes, TrxR1, TrxR2 and TrxR3, and selenoprotein P (SelP). Se deficiency reduced both enzyme activity and mRNA level of cGPx, but did not affect those of PHGPx. SelP mRNA level was also reduced by Se deficiency, although the extent of reduction was much smaller than that of cGPx mRNA. We further found that TrxR activity was also decreased by Se deficiency but none of the mRNA levels of TrxR isozymes were reduced. These results indicate that vascular endothelial cells express several selenoproteins including cGPx, PHGPx, TrxR isozymes and SelP which might play important roles in the defense system against oxidative stresses and that the expressions of these selenoproteins are differently regulated by Se status.
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PMID:Effects of selenium deficiency on expression of selenoproteins in bovine arterial endothelial cells. 1145 13

Bed rest is an integral part of treatment of numerous diseases. Typical examples are bone fractures of lower extremities and pelvis. Temporary immobilization is necessary also, e.g., in heart diseases (stroke), backbone and imminent abortion. The sick organism spares energy during the bed rest wich is beneficial. However, bed rest results in many alterations which are disadavantageous. They concern the function of almost all organs and systems but affect most significantly the locomotor and ciruclatory systems. Bed rest brings also about changes in the composition of peripheral blood and functions of the morphotic elements of blood. Red blood cells are subjected to the action of large amounts of reactive oxygen species (ROS). During oxidation of hemoglobin to methemoglobin superoxide radical anion (O2-) is formed: HbFe2+ + O2 --> MetHbFe3+ + O2- (1) Ferrous and ferric ions present in the cytoplasm of red blood cells may be catalysts of the Fenton reaction leading to the production of the hydroxyl radical: O2- + Fe3+ --> O2- + Fe2+ (2) Fe2+ + H2O2 --> Fe3+ + OH + HO- (3) OH shows a tremendous reactivity. It may react with lipids, proteins, nucleic acids and carbohydrates. The process of lipid peroxidation is best understood. It concerns mainly polyunsaturated fatty acids present in cell membranes. Peroxidation of membrane lipids decreases membrane fluidity and impairs its barrier function. The lowered membrane fluidity compromises erythrocyte deormability which in turn disturbs oxygen delivery to the tissues. End productions of lipid peroxidation are low-molecular wieght compounds, among them carbohydrates (ethane and pentane) and aldehydes, e.g. malondialdehyde (MDA). MDA concentration is an acknowldeged marker of the intensity of lipid peroxidation. Erythrocytes contain a complex system of protection against the action of ROS. It includes various enzymatic and non-enzymatic mechanism. The most important antioxidative enzymes of the red blood cells are superoxide dismutase (Cu,Zn-SOD, EC 1.15.1.1) catalase (CAT, EC 1.11.1.6) and glutathione peroxidase (GSH-Px, EC 1.11.1.9). Cu,Zn-SOD catalyzes the dismuation of O2- to hydrogen peroxide (H2O2). Catalase and peroxidase remove H2O2 and, moreover, GSH-Px can reduce lipid peroxides. Under normal conditions an equilibrium exists between the formation and removal ROS. If ROS are formed in excess or the defensive antioxidative mechanism are inefficient, oxidative stress develops. Derangement of the equilibrium between the formation and removal of ROS is important in the pathosgenesis of many diseases, e.g. atherosclerosis, diabetes, Down syndrome and Alzheimer disease. There are literature data on disturbances of enzymatic antioxidant defense mechanism of blood plateless during bed rest. This study was aimed at an examination of the post-traumatic bed rest on the enzymatic antioxidative defense mechanisms and lipid peroxidation in erythrocytes.
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PMID:Effect of long term bed rest in men on enzymatic antioxidative defence and lipid peroxidation in erythrocytes. 1154 39

To compare the chronic effect of several dialytic techniques (bicarbonate dialysis, BHD; acetate free biofiltration, AFB; hemodiafiltration, HDF; paired filtration dialysis, PFD) on atherosclerosis and antioxidant activity, three different indices were created. The first (atherosclerotic index = AI) is formed using the sum of three plasma substances: MDA, Hcy, and Cys (malondialdehyde, homocysteine, cysteine). The second (antioxidant activity index = AOAI) is the sum of five erythrocyte (E) parameters: E-GSH, GPx, CAT, SOD, GR (E-glutathione, E-glutathione peroxidase, E-catalase, E-superoxide dismutase, E-glutathione reductase). The third (defense index = DI) is derived from the previous two: (AOAI - AI). The indices were so expressed as AI in mmol/L, AOAI in U/g hemoglobin (Hb), and DI in arbitrary units. These indices were calculated in 20 controls and 51 chronic HD patients (26 female, 25 male) before, during, and after the first session of the week. HD patients were divided according to their dialytic technique: BHD, n = 35; AFB, n = 5 patients; HDF, n = 7 patients; or PFD = 4 patients. All patients had been treated with a given technique for at least 12 months, before entering the study. As expected, HD patients had AI values higher than controls, both before and after the session, with a mean value of 541 (before) and 331 (after), whereas controls had a mean value of 205. The AOAI was lower than controls, both before and after the session, the mean value being 1,122 (before) and 1,582 (after), that of controls being 2,424. In all cases, PFD gave the best "acute" results; at the end of a PFD session, near normal values of AI, AOAI, and DI (defensive index = AOAI - AI) were obtained.
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PMID:Do different dialytic techniques have different atherosclerotic and antioxidant activities? 1157 29

Extensive evidence suggests that reactive oxygen species are critically involved in the pathogenesis of cardiovascular diseases, such as atherosclerosis and myocardial ischemia-reperfusion injury. Consistent with this concept, administration of exogenous antioxidants has been shown to be protective against oxidative cardiovascular injury. However, whether induction of endogenous antioxidants by chemical inducers in vasculature also affords protection against oxidative vascular cell injury has not been extensively investigated. In this study, using rat aortic smooth muscle A10 cells as an in vitro system, we have studied the induction of cellular antioxidants by the unique chemoprotector, 3H-1,2-dithiole-3-thione [corrected] (D3T) and the protective effects of the D3T-induced cellular antioxidants against oxidative cell injury. Incubation of A10 cells with micromolar concentrations of D3T for 24 h resulted in a significant induction of a battery of cellular antioxidants in a concentration-dependent manner. These included reduced glutathione (GSH), GSH peroxidase, GSSG reductase, GSH S-transferase, superoxide dismutase, and catalase. To further examine the protective effects of the induced endogenous antioxidants against oxidative cell injury, A10 cells were pretreated with D3T and then exposed to either xanthine oxidase (XO)/xanthine, 4-hydroxynonenal, or cadmium. We observed that D3T pretreatment of A10 cells led to significant protection against the cytotoxicity induced by XO/xanthine, 4-hydroxynonenal or cadmium, as determined by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium reduction assay. Taken together, this study demonstrates for the first time that a number of endogenous antioxidants in vascular smooth muscle cells can be induced by exposure to D3T, and that this chemical induction of cellular antioxidants is accompanied by markedly increased resistance to oxidative vascular cell injury.
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PMID:Chemical induction of cellular antioxidants affords marked protection against oxidative injury in vascular smooth muscle cells. 1189 Jun 70

The purpose of this study was to investigate whether cholesterol plus methionine feeding may be a convenient model to produce atherosclerosis in rats, and also to examine the contribution of oxidative stress to this development. For this reason, lipid peroxide levels and antioxidant enzyme activities in the liver and aorta as well as histopathological findings were determined in male Wistar-albino rats fed a diet supplemented with cholesterol plus cholic acid and methionine for six months. This diet was found to increase lipid peroxide levels in the liver of rats. Hepatic glutathione peroxidase (GSH-Px) and catalase (CAT) activities increased, but superoxide dismutase (SOD) activity remained unchanged. In conclusion, cholesterol and methionine feeding in rats did not cause oxidative stress and atherosclerotic changes in the aorta, although hepatic prooxidant-antioxidant balance was affected by this diet.
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PMID:Cholesterol plus methionine feeding do not induce lipid peroxidation and atherosclerotic changes in the rat aorta. 1194 95

Wistar rats were fed Se-deficient (0.038 mg/kg diet) and adequate (0.326 mg/kg diet) diets for 13 weeks. The blood Se content, blood and vascular wall glutathione peroxidase (GPx) activity, serum high-density lipoprotein cholesterol (HDL-C) level and plasma prostacyclin (PGI(2)) concentration were decreased significantly, and the blood lipid peroxide (LPO) concentration, serum low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) level and plasma thromboxane A(2) (TXA(2)), content were increased significantly in Se-deficient rats compared with Se-adequate group, respectively. Furthermore the Se-deficient and adequate rats were given 5 mg/kg of cholestane-3 beta, 5 alpha, 6 beta -triol (3-triol) or vehicle only. Twenty four hours after treatment, the plasma PGI(2) level was decreased in Se-adequate rats infused 3-triol (+3 triol), meanwhile, the level in Se- deficient +3-triol group was much lower than that in Se-adequate +3-triol group. Compared with Se-adequate group, plasma TXA(2) content in Se-adequate +3-triol group had no significantly difference, but in Se- deficient rats infused 3-triol, plasma TXA(2) content was much higher than that in Se-adequate +3-triol group. The plasma ET concentration in Se-deficient group decreased slightly, but the concentration in Se-adequate +3-triol group increased significantly with respect to Se-deficient group. Although plasma ET concentration in Se-deficient group +3-triol did not increase, it was significantly lower than that in Se-adequate +3-triol group. The luminal surfaces of aorta thoracica of experimental rats were examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Observed by SEM, the luminal surface of aorta of Se-deficient rats showed few crater-like defects due to the disruption of endothelial cell. Se-adequate +3-triol group showed some crater-like defects on the their aorta luminal surface, but the luminal surface of Se-deficient +3-triol group exhibited numerous crater-like defects and appeared sponge-like as well as platelets adhering followed by thrombus formation in focal area of extensive endothelial damage. TEM studies also showed that the endothelium of aorta of Se deficient +3-triol group had more frequent lesion where endothelial cell plasma were swelling with profuse intracellular edema and some vacuoles were seen in cytoplasm. In severely injured areas, endothelial integrity was completely destroyed and smooth muscle cells were proliferating and migrated to the endomembrane. Thus, we can conclude that Se or selenoproteins in the vascular wall plays an important role in cytoprotection against cholesterol oxide-induced vascular damage in rats.
Atherosclerosis 2002 May
PMID:Role of selenium in cytoprotection against cholesterol oxide-induced vascular damage in rats. 1194 7

The effects of a red wine phenolic extract (PE) on plasma lipoproteins and early atherosclerosis were studied in hamsters. Hamsters (n = 32) were divided into 4 groups of 8 and fed an atherogenic diet for 8 wk. They received by force- feeding 7.14 mL/(kg. d) PE in 2.6 mol/L ethanol (E + PE) or PE in water (W + PE), mimicking a moderate consumption of red wine or alcohol-free red wine [30.4 mg/(kg. d)], or 2.6 mol/L ethanol (E-PE) or water (W-PE) as their respective controls. Plasma cholesterol and triglyceride concentrations were lower in groups that consumed PE. The decrease in plasma apolipoprotein (Apo) B concentration was due mainly to PE and was significantly lower in Group E + PE than in Group E-PE (-7.5%) and in Group W + PE than in Group W-PE (-40%). Apo-A1 was not affected. PE significantly increased plasma antioxidant capacity by 9% in Group E + PE and 18% in Group W + PE compared with their respective controls. Liver glutathione peroxidase activity was 67% greater in the group receiving PE in water compared with the group given water; there was no effect when PE was given in ethanol relative to its control. Aortic fatty streak area (AFSA) was significantly reduced in the groups receiving PE in ethanol (-32%) or PE in water (-29%) in comparison with their respective controls. Ethanol significantly reduced AFSA by 60% (Group E-PE vs. Group W-PE) or 62% (Group E + PE vs. Group W + PE). These data suggest that ethanol is a complementary component of phenolics in the benefits of red wine for hamsters and that chronic ingestion of PE in ethanol prevents the development of atherosclerosis through several mechanisms. With moderate consumption of red wine, ethanol can improve the effects of phenolic compounds. However, alcohol-free red wine appears to be a very good alternative to red wine.
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PMID:Red wine phenolic compounds reduce plasma lipids and apolipoprotein B and prevent early aortic atherosclerosis in hypercholesterolemic golden Syrian hamsters (Mesocricetus auratus). 1204 35

Oxidative stress, increased lipid peroxidation and decreased activity of antioxidant systems may contribute to the accelerated development of atherosclerosis in chronic renal failure patients during renal replacement therapy. The aim of the study was to investigate the influence of vitamin E (400 mg/day) on some antioxidant defense parameters in CAPD patients. In fourteen CAPD patients, erythrocyte antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), the concentration of plasma malondialdehyde (MDA), vitamin A, vitamin C and vitamin E were investigated. The study was divided into two periods. Each period lasted six weeks. In the first period patients received orally vitamin E 400 mg/day, in the second period they did not receive vitamin E or other antioxidant drugs. Each parameter was determined at the beginning of the study and at the end of each period. Six CAPD patients were treated by erythropoietin (EPO) and received orally pyridoxine 20 mg/day and the others without EPO treatment received pyridoxine 5 mg/day. Six-week treatment by vitamin E (400 mg/day) led to the significant increase of serum vitamin E (from 33.6+/-9.0 to 49.3+/-15.5 micromol/L) and to the significant decrease of MDA (from 2.62+/-0.5 to 2.36+/-0.4 micromol/L). The mean values of erythrocyte enzymes were in or under the lower margin of normal range and were not influenced by vitamin E in CAPD patients. The results of our study showed that orally administered vitamin E is a very important antioxidant agent for CAPD patients.
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PMID:Vitamin E as an antioxidant agent in CAPD patients. 1207 33


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