Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of myocardial infarction in patients who have the aquired immunodeficiency syndrome (AIDS) is increasing. However, no effective therapeutic agents have been discovered to reduce myocardial ischemia-reperfusion (I/R) injury in pathologies associated with AIDS. The aim of this study was to determine if infarct size is increased in murine AIDS after I/R injury and if I/R injury could be attenuated with vitamin E supplementation. Three groups of mice were studied: control, murine AIDS, and murine AIDS with vitamin E supplementation. Anesthetized mice were subjected to 30 min of left anterior descending coronary artery occlusion and 120 min of reperfusion. The hearts in mice that had murine AIDS had a larger infarct size compared to controls after I/R injury. Vitamin E supplementation significantly reduced infarct size and inhibited polymorphonuclear neutrophil (PMN) CD11b expression (p < 0.05). However, vitamin E supplementation did not affect PMN reactive oxygen species (ROS) production and platelet CD62p expression. These results suggest that the reduction of myocardial I/R injury with vitamin E supplementation may be the result of the inhibition of PMN CD11b expression. Vitamin E may be a promising prophylactic agent for the reduction of the severity of myocardial I/R injury in patients who have AIDS.
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PMID:Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS. 1227 Nov 55

The decreased oxidizability of plasma lipoproteins is related to the increased vitamin E intake and its association with a relatively lower incidence of coronary heart disease has been proposed. We investigated the effect of the in vivo vitamin E supplementation on the oxidizability of serum lipids in patients with ischemic heart disease and a moderate hypercholesterolemia. Thirty-two patients (16 males and 16 postmenopausal women) participated in this placebo-controlled, randomized trial. They were treated with 400 mg vitamin E/day for 6 weeks. The copper-induced serum lipid oxidizability ex vivo was assessed by measuring conjugated diene formation at 245 nm. We also measured vitamin E, malondialdehyde (MDA) and uric acid concentrations in the plasma. Because of observed significant differences in parameters of serum lipid oxidizability (lag time and maximal rate of oxidation), plasma alpha-tocopherol and MDA levels between male patients and postmenopausal women supplemented with vitamin E, the results were compared between both genders. Six weeks of vitamin E supplementation significantly increased plasma vitamin E levels (by 87 %) in male patients but in postmenopausal women only by 34 %. Concomitantly with increased plasma levels of vitamin E the decrease in plasma MDA levels was observed in male patients (decrease by 20 %; p=0.008), but in postmenopausal women the decrease did not attain statistical significance. Plasma uric acid levels were not apparently changed in placebo or vitamin E supplemented groups of patients. The changes in ex vivo serum lipid oxidizability after vitamin E, supplementation have shown a significantly prolonged lag time (by 11 %; p=0.048) and lowered rate of lipid oxidation (by 21 %; p=0.004) in male patients in comparison with postmenopausal women. Linear regression analysis revealed a significant correlation between plasma vitamin E levels and the lag time (r=0.77; p=0.03) and the maximal rate of serum lipid oxidation (r=-0.70; p=0.05) in male patients. However, in postmenopausal women the correlations were not significant. We conclude that 400 mg vitamin E/day supplementation in patients with ischemic heart disease and a moderate hypercholesterolemia influenced favorably ex vivo serum lipid oxidation of male patients when compared with postmenopausal women. The observed differences between both genders could be useful in the selection of the effective vitamin E doses in the prevention of coronary heart disease.
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PMID:Serum ex vivo lipoprotein oxidizability in patients with ischemic heart disease supplemented with vitamin E. 1247 Jan 98

In the 80's, retrospective studies showed an inverse relation between fish consumption and ischemic heart disease (IHD) mortality. In parallel, fish fats containing the polyunsaturated fatty acid (PUFA) eicosapentaenoic (EPA) were shown to impair platelet aggregation and thromboxane formation. The results of the large prospective trials, the Diet and Reinfarction Trial (DART) and the Lyon Heart Study in the secondary prevention of myocardial infarction, have further supported the interrelationships between diet and dietary prevention of IHD. In the DART Study, the cardioprotection by EPA was paralleled by an increase plasma content of EPA. In the Lyon, in addition to changes in the content of EPA, changes in other well known variables (i.e. leukocytes and vitamin E), often abnormal in subjects prone to arterial thrombosis, have been found. The GISSI Prevenzione Trial was a prospective, multicentric, open labeled trial with a factorial design, in which 11,324 recent (<3 mo) survivors of a first myocardial infarction were assigned to receive, in addition to the usual strategy, a supplementation of n-3 PUFA, vitamin E, or the combination of the two. Cardiovascular death (-30%), coronary heart disease death (-35%), total death (-20%) and sudden death (-45%) were all significantly reduced by the n-3 PUFA supplementation. The reduced tendency to sudden death of survivors of myocardial infarction on treatment with n-3 PUFA are in keeping with a series of scanty but reliable clinical data as well as of experimental studies. However, we believe that large-scale prospective multicentric randomized trials aimed at preventing sudden death in high-risk patients as well as at testing the effects of n-3 PUFA in patients with intracoronary devices and sustained ventricular arrhythmias, are a major direction to be followed to better understand the n-3 PUFA and sudden death issue.
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PMID:Polyunsaturated fatty acids, thrombosis and vascular disease. 1367 77

Reactive oxygen species-mediated cellular injury is involved in the pathogenesis of many diseases, including those affecting the cardiovascular system, such as myocardial ischemia-reperfusion injury, inflammation, and atheroscleosis. Raxofelast (IRFI-016; (+/-)-5-acetoxy-2, 3-dihydro-4, 6, 7-trimethyl-2-benzofuran-acetic acid) was designed with the aim of maximizing the antioxidant potency of phenols chemically related to vitamin E. The antioxidant activity of raxofelast has been convincingly demonstrated in several in vitro studies and in various models of ischemia-reperfusion injury. In this study, the antiproliferative effects of raxofelast were investigated to determine whether transduction signals and protooncogenes are affected in H(2)O(2)-stimulated rat aortic smooth muscle cells. In a tetrazolium-based colorimetric assay, the proliferation of rat aortic smooth muscle cells was increased by 3-fold in 0.1% fetal bovine serum/Dulbecco's modified Eagle's medium (DMEM) containing 500 microM H(2)O(2), indicating that exogenous 500 microM H(2)O(2) was a growth stimulator of rat aortic smooth muscle cells. Exogenous H(2)O(2) significantly activated extracellular signal-regulated kinases (ERKs) activity within 30 min and raxofelast inhibited the ERKs activation dose dependently in 500 microM H(2)O(2)-stimulated rat aortic smooth muscle cells (IC(50): 200 microM). Raxofelast reduced the intracellular reactive oxygen species generated by exogenous H(2)O(2) in a dose-dependent manner. In 500 microM H(2)O(2)-stimulated rat aortic smooth muscle cells, raxofelast dramatically attenuated the activation of mitogen-activating protein kinase (MAPK)/ERK kinase 1, 2 (MEK1,2) and protein kinase C (PKC) without affecting Ras expression. Induction of c-myc mRNA was significantly reduced dose dependently up to 100 microM by raxofelast in concentrations. These data indicate that the antiproliferative effects of raxofelast in H(2)O(2)-stimulated rat aortic smooth muscle cells may involve the suppression of intracellular reactive oxygen species formation and the inhibition of ERKs by inactivation through PKC and MEK1,2 and down-regulation of c-myc expression, regardless of Ras activation.
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PMID:Antiproliferative mechanisms of raxofelast (IRFI-016) in H2O2-stimulated rat aortic smooth muscle cells. 1474 95

The development of atherosclerosis is a multifactorial process in which both elevated plasma cholesterol levels and proliferation of smooth muscle cells play a central role. Numerous studies have suggested the involvement of oxidative processes in the pathogenesis of atherosclerosis and especially of oxidized low density lipoprotein. Some epidemiological studies have shown an association between high dietary intake and high serum concentrations of vitamin E and lower rates of ischemic heart disease. Cell culture studies have shown that alpha-tocopherol brings about inhibition of smooth muscle cell proliferation. This takes place via inhibition of protein kinase C activity. alpha-Tocopherol also inhibits low density lipoprotein induced smooth muscle cell proliferation and protein kinase C activity. The following animal studies showed that vitamin E protects development of cholesterol induced atherosclerosis by inhibiting protein kinase C activity in smooth muscle cells in vivo. Elevated plasma levels of homocysteine have been identified as an important and independent risk factor for cerebral, coronary and peripheral atherosclerosis. However the mechanisms by which homocysteine promotes atherosclerotic plaque formation are not clearly defined. Earlier reports have been suggested that homocysteine exert its effect via H2O2 produced during its metabolism. To evaluate the contribution of homocysteine in the pathogenesis of vascular diseases, we examined whether the homocysteine effect on vascular smooth muscle cell growth is mediated by H2O2. We show that homocysteine induces DNA synthesis and proliferation of vascular smooth muscle cells in the presence of peroxide scavenging enzyme, catalase. Our data suggest that homocysteine induces smooth muscle cell growth through the activation of an H2O2 independent pathway and accelerate the progression of atherosclerosis. The results indicate a cellular mechanism for the atherogenicity of cholesterol or homocysteine and protective role of vitamin E in the development of atherosclerosis.
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PMID:Molecular mechanisms of cholesterol or homocysteine effect in the development of atherosclerosis: Role of vitamin E. 1475 78

Free radicals pay an important role in the pathogenesis of atherosclerosis by their direct toxic action on the vascular endothelium as well as by antioxidant of low density lipoproteins (LDL) which subsequently increase their atherogenic potential. Natural antioxidants interrupt the chain-like increase of radicals and thus also the risk of oxidation stress. The majority of epidemiological data indicate that an increased intake of fruit, vegetables and other foods of plant origin reduces the risk of cardiovascular disease. On the other hand, several so far not completed long-term intervention studies with some antioxidant vitamins (e. g. vitamin E, beta-carotene) don't provide such unequivocal results. This indicated that fruit and vegetables contain other protective substances, other than vitamins, some which were identified so far. It is beyond doubt than even the intake of very large amounts of antioxidant vitamins does not ensure in humans exposed to the potent action of several traditional cardiovascular risk factors (hypertension, high LDL-cholesterol, smoking) unequivocal protection against ischaemic heart disease. On the other hand, it is probable that chronic antioxidant deficiency enhances the risk of development of pathological changes of the vascular system. So far the problem has yet been resolved whether to recommend within the framework of cardiovascular disease prevention to the public at large daily consumption of preparations containing natural antioxidants. The final word on the effectiveness of antioxidants in the prevention of cardiovascular disease will be provided by extensive intervention studies which are at present under way, the results of which will be available within the few years.
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PMID:[Effect of free radicals and antioxidant on the vascular wall]. 1564 43

The study of oxidative contributions to aging has reached sufficient maturity to support the development of interventional strategies designed to forestall or reverse protein cross-linking, oxidation of DNA and lipids, and mitochondrial senescence associated with chronic pathology and aging. Catalytic antioxidants, including combined superoxide dismutase (SOD) and catalase mimics, extend the lifespan of oxidatively compromised animals such as Mn-SOD knockout mice, and will be entering the clinic for radiation-induced dermatitis. Substituted phenacylthiozolium compounds that slow the formation and break extant protein cross-linkages formed via Maillard reactions, restoring vascular compliance in aged animals, and are showing efficacy in clinical trials. Non-feminizing estrogen analogs (eg, 17- alpha estradiol) block cytotoxicity in a host of oxidative stress models and moderate neuronal loss in MCAO stroke models. Efficacy of the polycyclic phenols is synergistically amplified by glutathione supplementation, suggesting that the two function as a redox couple analogous to vitamin E and ascorbate. Finally, discovery of novel small molecules designed to stabilize mitochondrial function during Ca(2+)-induced oxidative stress, such as that occurring during stroke or myocardial ischemia reperfusion, will be accelerated by a proprietary fluorescence resonance energy transfer assay developed at MitoKor. Maintaining mitochondrial function under these circumstances will improve cellular bioenergetic and oxidative status, and hence moderate secondary necrosis and apoptosis.
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PMID:Oxidative Stress and Aging - Second International Conference. Technologies for assessment and intervention strategies. 2-5 April 2001, Maui, USA. 1599 30

Vegetarian diets do not contain meat, poultry or fish; vegan diets further exclude dairy products and eggs. Vegetarian and vegan diets can vary widely, but the empirical evidence largely relates to the nutritional content and health effects of the average diet of well-educated vegetarians living in Western countries, together with some information on vegetarians in non-Western countries. In general, vegetarian diets provide relatively large amounts of cereals, pulses, nuts, fruits and vegetables. In terms of nutrients, vegetarian diets are usually rich in carbohydrates, n-6 fatty acids, dietary fibre, carotenoids, folic acid, vitamin C, vitamin E and Mg, and relatively low in protein, saturated fat, long-chain n-3 fatty acids, retinol, vitamin B(12) and Zn; vegans may have particularly low intakes of vitamin B(12) and low intakes of Ca. Cross-sectional studies of vegetarians and vegans have shown that on average they have a relatively low BMI and a low plasma cholesterol concentration; recent studies have also shown higher plasma homocysteine concentrations than in non-vegetarians. Cohort studies of vegetarians have shown a moderate reduction in mortality from IHD but little difference in other major causes of death or all-cause mortality in comparison with health-conscious non-vegetarians from the same population. Studies of cancer have not shown clear differences in cancer rates between vegetarians and non-vegetarians. More data are needed, particularly on the health of vegans and on the possible impacts on health of low intakes of long-chain n-3 fatty acids and vitamin B(12). Overall, the data suggest that the health of Western vegetarians is good and similar to that of comparable non-vegetarians.
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PMID:Health effects of vegetarian and vegan diets. 1644 42

Ischemic heart disease (IHD) has now assumed a global dimension. It still remains one of the major health problems not only in the advanced countries, but also, is becoming a serious health issue in the developing and the economically weaker countries. Apart from other factors, changing economic scenario, stress and strain in daily life as well as altered dietary habits in the populations appear responsible for the increased incidence of cardiovascular disease (CVD). The treatment modalities, invasive, non-invasive and pharmacological are economically no dearer, even to population of affluent countries. Likewise, treatment costs of serious cardiovascular diseases are becoming difficult to be borne by population of the developing nations. Prevention of IHD would be a better way to protect the population from physical and economic disaster. The current article comprehensively describes the relation between oxidative stress and cardiac disease, explains the direct effect of reactive oxygen species on cardiac function and projects how the use of vitamin E can be of benefit in the prevention of IHD with concluding remarks highlighting the need for inclusion of a fruit and vegetable rich diet and regular exercise to keep the dearer heart active and healthy.
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PMID:Vitamin E in the prevention of ischemic heart disease. 1670 19

Vitamin E has the ability to scavenge a wide spectrum of free radicals, including singlet oxygen, superoxide, and hydroxyl radicals. It has beneficial effects against several other disorders, such as atherosclerosis and ischemic heart disease, because it acts as a transcriptional regulator for gene expression via a transcription factor TAP. The beneficial effect of vitamin E on plasma insulin and glucagon levels was examined using radioimmunoassay technique. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin at a dose of 60 mg/kg body weight. Vitamin E was given at a dose of either 0.2 mg, 0.4 mg, or 0.8 mg per animal 10 days before and after the onset of diabetes. Vitamin E significantly (P < 0.05) increased plasma insulin levels in normal rats but failed to increase the plasma insulin level in diabetic rats. In contrast, vitamin E caused a significant (P < 0.05) reduction in plasma glucagon level in rats treated before and after the onset of diabetes. Vitamin E may ameliorate some diabetic complication via reduction in the level of circulating glucagon.
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PMID:Vitamin E decreases the hyperglucagonemia of diabetic rats. 1715 20


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