Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postmenopausal women experiencing hot flashes in whom estrogen replacement is contraindicated have alternatives available to them; however, there is no clearly defined treatment modality. The literature addressing many of these alternatives has serious limitations, which include the small number of women enrolled and lack of comparative studies between agents. Each patient needs to be assessed in terms of her current medical status, concomitant medications, and the degree to which vasomotor instability interferes with everyday activities. The literature suggests that megestrol acetate 20 mg bid may provide significant relief. Women who opt to use megestrol acetate must be told in advance that the effects will not be felt immediately particularly if tamoxifen is used concomitantly. Clonidine and medroxyprogesterone may constitute potential alternatives, but patients may not be able to tolerate the adverse effects. Because of the lack of literature supporting their clinical use, options such as vitamin E and ginseng need to be approached cautiously. Exercise has a role in alleviating some of the complications associated with menopause, such as heart disease and osteoporosis, but its effect on neurotransmitters and hormone concentrations, and how this relates to the treatment of hot flashes have not been characterized. Patients should be told that regular physical activity, a balanced diet, avoidance of alcohol and caffeine, and stress reduction may be of additional help in decreasing vasomotor flushing.
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PMID:Alternatives to estrogen for the treatment of hot flashes. 922 57

In this study, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) levels were measured in heart tissues from guinea pigs treated with gentamicin and gentamicin plus vitamin E combination. Mean values were compared with those of the controls treated with only physiological saline solution. The activities of SOD and GSH-Px were found to be lower and the MDA level higher in the hearts from gentamicin-treated animals compared with those of the controls. In the gentamicin plus vitamin E group, however, tissue SOD activity was found to be increased and MDA level decreased significantly relative to the gentamicin group. GSH-Px activity was lowest in this group. Results suggest that gentamicin suppresses SOD and GSH-Px activities in heart tissue, thereby making the tissue more vulnerable to oxidative stress and peroxidative attacks, an important indicator of which is increased MDA level in the heart tissues from gentamicin-treated guinea pigs. This effect might be deleterious when gentamicin is used after cardiac surgery since a potential risk of free radical injury exists in the heart tissue during and/or after cardiac surgery owing to ischaemia and reperfusion processes, and, possibly, in the management of the patients with certain types of heart disease. Our results showed that vitamin E given concomitantly with gentamicin could protect the heart tissue against free radical injury.
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PMID:The effects of gentamicin on the activities of glutathione peroxidase and superoxide dismutase enzymes and malondialdehyde levels in heart tissues of guinea pigs. 952 93

The 'antioxidant hypothesis' proposes that vitamin C, vitamin E, carotenoids, and other antioxidants occurring in fruit and vegetables afford protection against heart disease and cancer by preventing oxidative damage to lipids and to DNA, respectively. To test elements of this hypothesis, we have measured blood levels of dietary antioxidants, and 8-oxodeoxyguanosine (8-oxo-dG) concentrations in lymphocyte DNA, in healthy men and women from five European countries: France, Ireland, The Netherlands, Spain, and the U.K. Volunteers, aged 25 45, all nonsmokers, gave blood samples before and after a 12-wk carotenoid supplementation regime. Vitamin C was measured in plasma and vitamin E and carotenoids were measured in serum by high-performance liquid chromatography (HPLC). 8-oxo-dG was assayed by HPLC (with coulometric detection) in DNA isolated from lymphocytes from the same blood samples. Mean values were calculated for groups of volunteers at each sampling time according to country, sex, and supplementation (between 9 and 24 individual samples contributing to each mean). We found that 8-oxo-dG levels in lymphocyte DNA vary significantly according to sex and country. A low mean 8-oxo-dG concentration is seen in DNA of women from all five countries, and of men from France and Spain. 8-oxo-dG is significantly higher (up to about threefold) in lymphocyte DNA from men in Ireland and the U.K. Oxidative DNA damage is not significantly affected by carotenoid supplementation; nor is there any association with mean baseline levels of antioxidants, which are generally similar in the five countries. The five countries sampled lie on an axis from northern to southern Europe with a steep gradient in terms of premature heart disease. There is a strong association between premature coronary heart disease mortality in men and the mean levels of 8-oxo-dG for the five countries (r = 0.95, P < 0.01). Women have low coronary heart disease mortality rates, which do not correlate with 8-oxo-dG. In terms of cancer deaths, only colorectal cancer in men shows a significant positive correlation (r = 0.91, P < 0.05), and stomach cancer in women is negatively correlated with DNA oxidation (r = -0.92, P = 0.01).
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PMID:Oxidative DNA damage measured in human lymphocytes: large differences between sexes and between countries, and correlations with heart disease mortality rates. 976 83

Vitamin E was advocated as an effective treatment for heart disease by Dr. Even Shute of London, Ontario more than 50 years ago. His pioneering claims, which were unacceptable to the medical community at large, have been confirmed by recent findings from epidemiologic studies and clinical trials. This review integrates our current knowledge of atherogenesis with the biological functions of vitamin E. The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.
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PMID:Vitamin E and atherosclerosis. 977 22

The impact of diet and specific food groups on aging and age-associated degenerative diseases has been widely recognized in recent years. The modern concept of the free radical theory of aging takes as its basis a shift in the antioxidant/prooxidant balance that leads to increased oxidative stress, dysregulation of cellular function, and aging. In the context of this theory, antioxidants can influence the primary "intrinsic" aging process as well as several secondary age-associated pathological processes. For the latter, several epidemiological and clinical studies have revealed potential roles for dietary antioxidants in the age-associated decline of immune function and the reduction of risk of morbidity and mortality from cancer and heart disease. We reported that long-term supplementation with vitamin E enhances immune function in aged animals and elderly subjects. We have also found that the beneficial effect of vitamin E in the reduction of risk of atherosclerosis is, in part, associated with molecular modulation of the interaction of immune and endothelial cells. Even though the effects of dietary antioxidants on aging have been mostly observed in relation to age-associated diseases, the effects cannot be totally separated from those related to the intrinsic aging process. For modulation of the aging process by antioxidants, earlier reports have indicated that antioxidant feeding increased the median life span of mice to some extent. To further delineate the effect of dietary antioxidants on aging and longevity, middle-aged (18 mo) C57BL/6NIA male mice were fed ad libitum semisynthetic AIN-76 diets supplemented with different antioxidants (vitamin E, glutathione, melatonin, and strawberry extract). We found that dietary antioxidants had no effect on the pathological outcome or on mean and maximum life span of the mice, which was observed despite the reduced level of lipid peroxidation products, 4-hydroxynonenol, in the liver of animals supplemented with vitamin E and strawberry extract (1.34 +/- 0.4 and 1.6 +/- 0.5 nmol/g, respectively) compared to animals fed the control diet (2.35 +/- 1.4 nmol/g). However, vitamin E-supplemented mice had significantly lower lung viral levels following influenza infection, a viral challenge associated with oxidative stress. These and other observations indicate that, at present, the effects of dietary antioxidants are mainly demonstrated in connection with age-associated diseases in which oxidative stress appears to be intimately involved. Further studies are needed to determine the effect of antioxidant supplementation on longevity in the context of moderate caloric restriction.
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PMID:The effect of long-term dietary supplementation with antioxidants. 992 43

Vitamin E is one of the most researched compounds in medicine. Vitamin E is actually a general name for potentially eight different compounds, so supplements can contain several forms and vitamin E in the diet also differs from the form found over the counter. There has been a strong interest in this supplement in the prostate cancer arena primarily because of a Finnish study that demonstrated a lower morbidity and mortality from this disease in men taking 50 mg of synthetic (alpha-tocopherol) vitamin E daily. In addition, observations from laboratory and clinical studies dealing with heart disease have found that gamma-tocopherol may also play a significant role in prevention; therefore, we decided to test the ability of this compound (versus synthetic vitamin E) to control the growth of a human prostate cancer cell line. Gamma-tocopherol was found to be superior to alpha-tocopherol in terms of cell inhibition in vitro. Both forms of vitamin E (and others) should be thoroughly evaluated in the future to provide the most effective chemoprevention information to the patient.
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PMID:Vitamin E, alpha- and gamma-tocopherol, and prostate cancer. 1033 21

A growing amount of scientific evidence supports the participation of oxygen radicals in heart disease and, consequently, a protective effect of vitamin E (VE), beta-carotene (BC), and other antioxidants. The aim of this study was to correlate plasma VE and BC concentration with the clinical course of the acute myocardial infarction (AMI). We evaluated 120 patients that were admitted at the coronary units within 12 h after the development of AMI symptoms. The AMI was diagnosed by clinical and biochemical criteria and by electrocardiography and echocardiography. Plasma VE and BC concentration was determined by high performance liquid chromatography. The patients were separated according to the plasma concentration of VE (group H, VE > 17.5 microM; group L, VE < 17.5 microM). Clinical history of patients, age, sex, associated cardiovascular risk factors, AMI localization, hemodynamic class, and the treatment received were similar between different groups. The blood levels of creatine phosphokinase (CK) evaluated either 24- or 48-h after admittance, were higher in group L than in group H (24 h: H = 436 +/- 31 U/ml vs. L = 642 +/- 84 U/ml; p < .005; 48 h: H = 242 +/- 21 U/ml; L = 423 +/- 82 U/ml, p < 0.005). The number of deflexions in the electrocardiogram at admittance (ECG-D) was significantly higher in group L than in group H (4.7 +/- 0.3 vs. 3.7 +/- 0.2; p < .005). The number of new Q waves in the ECG of release (ECG-Q) was higher in group L than in group H (2.9 +/- 0.3 vs. 2.2 +/- 0.2; p < .05). The number of segments affected in the echocardiograms (EC-S) was: L = 5.3 +/- 0.6 vs. H = 4.4 +/- 0.2; p = 0.11. No significant differences in CK levels, ECG-D, ECG-Q, and EC-S were observed when the patients were separated according their plasma BC levels. These results indicate that a high concentration of plasma VE, but not BC, was associated with a diminution in the creatine phosphokinase release and with the AMI extension.
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PMID:Tissue damage in acute myocardial infarction: selective protection by vitamin E. 1040 25

A review is presented of studies on the effects of vitamin E on heart disease, studies encompassing basic science, animal studies, epidemiological and observational studies, and four intervention trials. The in vitro, cellular, and animal studies, which are impressive both in quantity and quality, leave no doubt that vitamin E, the most important fat-soluble antioxidant, protects animals against a variety of types of oxidative stress. The hypothesis that links vitamin E to the prevention of cardiovascular disease (CVD) postulates that the oxidation of unsaturated lipids in the low-density lipoprotein (LDL) particle initiates a complex sequence of events that leads to the development of atherosclerotic plaque. This hypothesis is supported by numerous studies in vitro, in animals, and in humans. There is some evidence that the ex vivo oxidizability of a subject's LDL is predictive of future heart events. This background in basic science and observational studies, coupled with the safety of vitamin E, led to the initiation of clinical intervention trials. The three trials that have been reported in detail are, on balance, supportive of the proposal that supplemental vitamin E can reduce the risk for heart disease, and the fourth trial, which has just been reported, showed small, but not statistically significant, benefits. Subgroup analyses of cohorts from the older three trials, as well as evidence from smaller trials, indicate that vitamin E provides protection against a number of medical conditions, including some that are indicative of atherosclerosis (such as intermittent claudication). Vitamin E supplementation also produces an improvement in the immune system and protection against diseases other than cardiovascular disease (such as prostate cancer). Vitamin E at the supplemental levels being used in the current trials, 100 to 800 IU/d, is safe, and there is little likelihood that increased risk will be found for those taking supplements. About one half of American cardiologists take supplemental vitamin E, about the same number as take aspirin. In fact, one study suggests that aspirin plus vitamin E is more effective than aspirin alone. There are a substantial number of trials involving vitamin E that are in progress. However, it is possible, or even likely, that each condition for which vitamin E provides benefit will have a unique dose-effect curve. Furthermore, different antioxidants appear to act synergistically, so supplementation with vitamin E might be more effective if combined with other micronutrients. It will be extremely difficult to do trials that adequately probe the dose-effect curve for vitamin E for each condition that it might affect, or to do studies of all the possible combinations of other micronutrients that might act with vitamin E to improve its effectiveness. Therefore, the scientific community must recognize that there never will be a time when the science is "complete." At some point, the weight of the scientific evidence must be judged adequate; although some may regard it as early to that judgement now, clearly we are very close. In view of the very low risk of reasonable supplementation with vitamin E, and the difficulty in obtaining more than about 30 IU/day from a balanced diet, some supplementation appears prudent now.
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PMID:Vitamin E and heart disease: basic science to clinical intervention trials. 1065

Three large-scale clinical trials tested the effects of supplemental beta-carotene on the risk for chronic diseases such as cancer. The populations involved were Finnish male heavy smokers (the Alpha Tocopherol Beta Carotene [ATBC] trial), male asbestos workers and male and female heavy smokers (Beta-Carotene and Retinol Efficacy Trial [CARET]), and U.S. male physicians, 11% of whom were current smokers (Physician's Health Study). All three trials concluded that beta-carotene provided no protection against lung cancer; however, quite unexpectedly, two of the trials found a higher risk for lung cancer for those subjects given beta-carotene compared with those that were not. Several authors concluded from these beta-carotene trials that the protective effects of antioxidants against chronic disease are not as great as had been hoped. As reviewed here, however, beta-carotene may or may not be an antioxidant; it certainly differs in many respects from the prototypical antioxidant, vitamin E. In any case, the majority of beta-carotene's effects in vivo are probably not derived from any antioxidant properties that it may possess, but rather from its effect on a number of biochemical systems. Whether taking supplemental antioxidants can reduce the risk for chronic diseases remains to be established, although the case for vitamin E and heart disease appears strong. However, the association between eating a diet sufficient in fruits and vegetables and reduced risk for a number of diseases is consistent. There is no evidence at present that consuming small amounts of supplemental beta-carotene, i.e., amounts in foods or in a multivitamin tablet, is unwise for any population. The role of supplementation, however, particularly at high levels, with compounds that may be anti-oxidants but that are less well understood than vitamin E (e.g., carotenoids, plant polyphenols, and other phytochemicals), is less clear. The surprising results of the ATBC and CARET trials are a red flag, signaling the need for further research; a number of areas for future work are suggested here. Future research should lead to a clearer understanding of the effects of beta-carotene and other phytochemicals, as well as to more refined strategies for intervention, with important clinical and public health implications.
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PMID:Beta carotene: from biochemistry to clinical trials. 1074 8

The generation of reactive oxygen species (ROS) is associated with life in aerobic conditions. ROS are thought to be implicated in the pathogenesis of various human diseases since they are capable of damaging biological macromolecules such as DNA, carbohydrates and proteins. The organism maintains defense against ROS, including enzymes and low molecular-weight antioxidants. An important source of antioxidants is diet which contains numerous compounds exhibiting antioxidant activity. A shortage of antioxidants in the diet might promote coronary heart disease through accumulation of oxidized LDL in macrophages. However, antioxidants may also influence endothelial functions, smooth muscle cell proliferation, thrombosis and plaque rupture. Consumption of fruits and vegetables, olive oil, red wine and tea is inversely correlated with heart disease rates. These foods are particularly rich in natural antioxidant nutrients, including ascorbate (vitamin C), the tocopherols (vitamin E) and carotenoids. More than 600 naturally occurring carotenoids have been identified. These compounds are plant pigments that provide the bright color of various fruits and vegetables; lycopene, which gives tomatoes their red color, is under active research. Flavonoids are > 4,000 naturally occurring substances which provide color, texture and taste for plant foods. As free radical scavengers, flavonoids inhibit lipid peroxidation, promote vascular relaxation and help prevent atherosclerosis. A sufficient supply with antioxidants from diet might help prevent or delay the occurrence of pathological changes associated with oxidative stress. When diet fails to meet the antioxidant requirement, dietary supplements might be indicated. The recently coined term nutriceuticals describes a variety of nonprescription products that are used to enhance health. The best known are vitamin E, vitamin C, carotenoids, coenzyme Q10, flavonoids and the amino acid L-arginine. Rigorous clinical trials, particularly among high-risk groups, are needed before they can be recommended routinely to patients.
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PMID:Dietary antioxidants for cardiovascular prevention. 1081 86


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