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)

Fasting blood samples taken from 116 apparently healthy men aged 30-50 years were assayed for selenium, glutathione peroxidase activity, vitamin E, cadmium, lead, glucose, lipids, and albumin. Blood pressure was measured in each subject, and details of height, weight, smoking habits, and alcohol consumption were recorded. Multivariate analysis of the data showed that the decrease in blood and serum concentrations of selenium and the increase in whole blood cadmium concentrations in the cigarette smokers was independent of alcohol consumption. There was no correlation between blood selenium concentrations or glutathione peroxidase activities and the risk factors for cardiovascular disease. Neither alcohol consumption nor smoking had an effect on the vitamin E concentrations. There was a strong association, however, between vitamin E and serum lipid concentrations, although the increase in triglyceride concentrations in the smokers was not matched by a comparable increase in vitamin E. The possible role of selenium in the aetiology of heart disease remains unresolved.
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PMID:Selenium and vitamin E in relation to risk factors for coronary heart disease. 669 79

Great differences in dietary selenium intake have resulted in naturally occurring human selenium deficiencies and toxicities in certain parts of the world. Most North American diets, however, provide levels of selenium that fall within the estimated safe and adequate range of intake (50 to 200 microgram/day for adults) as established by the U.S. National Research Council. Low selenium status may develop in individuals fed certain therapeutic diets or given total parenteral nutrition. Attempts have been made to link low selenium intake with cancer and heart disease, but additional research is needed in this area. Selenium, as a constituent of glutathione peroxidase, plays a role in the antioxidant defense systems of the body, but other metabolic roles for selenium may yet be discovered.
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PMID:Clinical consequences of low selenium intake and its relationship to vitamin E. 681 23

Copper is an essential trace element and has profound influence on cardiac myopathy and heart metabolism. Dietary Cu restriction in rats results in cardiomyopathy, and affects the integrity of the basal lamina of cardiac myocytes and capillaries. Decreased levels of delta subunits of ATP synthetase and nuclear encoded subunits of cytochrome oxidase system have been observed. Alteration in expression of glutathione peroxidase and catalase in heart and liver in Cu deficiency (Cu-) has been noted involving both transcriptional and post transcriptional mechanisms. A short description of two genetically inherited disorders of Cu metabolism, i.e. Wilson's disease and Menkes' disease, and Indian childhood cirrhosis (environmental and/or genetic) have been included to illustrate that advances in the knowledge of Cu cellular transport gives a better understanding of the molecular basis of the pathophysiology of these diseases. Menkes' disease, a human model of defective Cu transport and Cu- has shown many pathological changes, similar to those of heart disease in Cu-. The recent cloning of four genes of putative Cu pumping ATPases (Cu-ATPases) from widely different sources, i.e. two from Enterococcus hirae and one each from Wilson's and Menkes disease patients (which are defective in Cu transport and metabolism), has opened a new chapter in the study of Cu cellular transport and metabolism. The encoded gene products, i.e. Cu-ATPases, show extensive homology and are members of a new class of ATP-driven Cu pumps involved in regulation of cellular Cu. Further, Cu transport by Cop B-ATPase (E. hirae) in membrane vesicles and in isolated rat liver plasma membrane has provided biochemical evidence of its role in ATP-driven Cu transport. In this short review I have critically examined the current evidence of the molecular basis of the pathophysiology of cardiomyopathy in Cu- and, have indicated the possible role of P-type Cu ATPase which may be one of the obligatory factors contributing to cardiomyopathy in experimental animals and probably humans. Experimental verification of this hypothesis will be the aim of future studies.
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PMID:Copper deficiency and heart disease: molecular basis, recent advances and current concepts. 945 22

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

Selenium, long recognised as an important 'dietary antioxidant', is now known to be an essential component of the active sites of a number of enzymes, including the glutathione peroxidase selenoenzyme family which scavenge hydroperoxides to prevent cellular damage. Dietary selenium deficiency has been linked to diseases as diverse as cancer, heart disease, arthritis and AIDS, and epidemiological evidence is now emerging for the beneficial effects of selenium supplementation. Thus, the pharmacology, biology and biochemistry of selenium metabolism have become subjects of considerable interest, which are spurring efforts to develop synthetic selenium-containing compounds as potential therapeutic agents. Phenylaminoalkyl selenides were developed in the authors' laboratories as novel, selenium-based pharmacological agents. We demonstrated that these compounds exhibited dose-dependent antihypertensive activity in spontaneously hypertensive rats. Biochemical studies established that as a consequence of the redox properties of their selenium moieties, these phenylaminoalkyl selenides possessed the remarkable property of propagating a cycle of turnover-dependent local depletion of reduced ascorbate when processed by the key enzyme of catecholamine metabolism, dopamine-beta-monooxygenase. On the basis of inductively coupled plasma/mass spectroscopic analyses, corroborated by operant behaviour and locomotor activity investigations, an orally-active phenylaminoalkyl selenide with restricted CNS permeability was successfully developed. To our knowledge, this compound--4-hydroxy-alpha-methyl-phenyl-2-aminoethyl selenide--is the first orally active, selenium-based anti-hypertensive compound ever reported. In the future, we anticipate more widespread efforts to incorporate selenium into rationally designed pharmaceutical agents, with the goal of developing novel compounds which may be of therapeutic benefit toward a variety of human diseases.
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PMID:Selenium-based antihypertensives. Rationale and potential. 987 85

Resveratrol (trans-3,4',5-trihydroxystibene) is a phytopolyphenol isolated from the seeds and skins of grapes. Recent studies indicate that resveratrol can block the process of multistep carcinogenesis, namely, tumor initiation, promotion and progression. Resveratrol can also reduce the risk of cardiovascular disease in man. The molecular mechanisms of resveratrol in chemoprevention of cancer and cardiovascular disease are interesting and under intensive investigation. Resveratrol was found to strongly inhibit nitric oxide (NO) generation in activated macrophages, as measured by the amount of nitrite released into the culture medium, and resveratrol strongly reduced the amount of cytosolic inducible nitric oxide synthase (iNOS) protein. The activation of nuclear factor kappa B (NF kappa B) induced by lipopolysaccharide (LPS) was inhibited by resveratrol. The phosphorylation and degradation of nuclear factor inhibitor kappa B alpha (I kappa B alpha) were inhibited by resveratrol simultaneously. Reactive oxygen species (ROS) are regarded as having carcinogenic potential and have been associated with tumor promotion. Resveratrol may act as a reactive oxygen species scavenger to suppress tumor development. In addition, resveratrol may block multistep carcinogenesis through mitotic signal transduction blockade. Reactive oxygen species are pivotal factors in the genesis of heart disease. Meanwhile, efficient endogenous antioxidants, including superoxide dismutase (SOD), glutathione peroxidase (GSHPx), and catalase, are present in tissues. A fine balance between reactive oxygen species and endogenous antioxidants is believed to exist. Any disturbance of this balance in favor of reactive oxygen species causes an increase in oxidative stress and initiates subcellular changes, leading to cardiomyopathy and heart failure. The experimental results indicate that exogenous antioxidant resveratrol is of value in chemopreventing the development of heart disease. It is urgent that more efforts be made to investigate newer therapies employing antioxidants for the chemoprevention of cardiovascular disease and cancer.
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PMID:Chemoprevention of cancer and cardiovascular disease by resveratrol. 1049 90

1. Gavage administration of the natural flavonoids tangeretin, chrysin, apigenin, naringenin, genistein and quercetin for 2 consecutive weeks to the female rat resulted in differential effects on selected phase 1 and 2 enzymes in liver, colon and heart as well as antioxidant enzymes in red blood cells (RBC). 2. Glutathione transferase (GST) activity assayed by use of the substrate 1-chloro-2,4-dinitrobenzene was significantly induced by apigenin, genistein and tangeretin in the heart but not in colon or liver. 3. In RBC chrysin, quercetin and genistein significantly decreased the activity of glutathione reductase (GR), catalase (CAT) and glutathione peroxidase (GPx), whereas superoxide dismutase (SOD) was only significantly decreased by genistein. 4. The oxidative status of the animal, measured as plasma malondialdehyde, revealed that chrysin, quercetin, genistein, and beta-naphthoflavone (BNF) significantly protected against, 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP)-induced oxidative stress. Hepatic PhIP-DNA adduct formation was not affected by any of the administered flavonoids, whereas PhIP-DNA adduct formation in colon was slightly, but significantly, inhibited by quercetin, genistein, tangeretin and BNF. 5. The observed effects of chrysin, quercetin and genistein on antioxidant enzymes, concurrently with a protection against oxidative stress, suggest a feedback mechanism on the antioxidant enzymes triggered by the flavonoid antioxidants. 6. Despite the use of high flavonoid doses, which by far exceed the human exposure levels, the effect on drug metabolizing and antioxidant enzymes was still very minor. The role of singly administered flavonoids in the protection against cancer and heart disease is thus expected to be limited.
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PMID:Differential effects of dietary flavonoids on drug metabolizing and antioxidant enzymes in female rat. 1064 9

Selenium is an essential trace element that is an integral part of many proteins, with catalytic and structural functions. The antioxidant properties of some selenoproteins, such as glutathione peroxidase, may be particularly important in carcinogenesis and heart disease. The content of selenium in food depends on the selenium content of the soil where the plants are grown or the animals are raised. Moreover, the metabolism of selenium is determined by its dietary form: some forms are better utilized than others. Therefore, wide variations have been found in selenium status in different parts of the world. In animal studies, selenium deficiency is associated with cardiomyopathy and sudden death, as well as reduced T-cell counts and impaired lymphocyte proliferation and responsiveness. Abnormalities in liver function, brain, heart, striated muscle, pancreas and genital tract have also been reported. In humans, selenium deficiency has been implicated in the etiology of cardiovascular disease and other conditions in which oxidative stress and inflammation are prominent features, but there is still only limited evidence from epidemiological and ecological studies for this, and the therapeutic benefit of selenium administration in the prevention and treatment of cardiovascular diseases remains insufficiently documented. Interventions studies are currently in progress to assess the benefits of selenium supplements in primary and secondary prevention of atherosclerosis. The results to date are inconclusive and further controlled trials are needed.
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PMID:The controversy surrounding selenium and cardiovascular disease: a review of the evidence. 1255 53

Coenzyme Q10 (CoQ10) is synthesized by the human body and found in certain foods. Daily supplementation of CoQ10 could protect against heart disease but the bioavailability of CoQ10 supplements depends on the formulation taken. We compared the bioavailability and antioxidant properties of two commercial CoQ10 formulations, a commercial grade CoQ10 powder (commercial grade CoQ) and a new BT-CoQ10 BIO-TRANSFORMED (BT-CoQ10) obtained by fermentation of a soy-based, CoQ10-rich media with baker's yeast. Eleven healthy individuals participated in a randomized two-way crossover trial, with a 3-week washout period. Capsules containing 300 mg of either BT-CoQ10 or commercial grade CoQ10 were given daily for 1 week and multiple blood samples were taken for CoQ10, glutathione and glutathione peroxidase (GPx) determination. In 3 subjects, baseline plasma CoQ10 levels were lower prior to BT than prior to commercial grade CoQ treatment. In the remaining participants, ingestion of BT vs. commercial grade CoQ significantly increased maximum plasma CoQ10 concentration (+126%, p = 0.04) and tended to increase CoQ10 area under the curve from 0 to 24 h (+160%, p = 0.07). One week of treatment with each formulation increased plasma CoQ10 but did not alter plasma glutathione or GPx activity. The enhanced bioavailability of the BT product might be due to its predominantly reduced, hydrophilic membrane-complex form.
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PMID:Relative bioavailability and antioxidant potential of two coenzyme q10 preparations. 1262 83

Selenium is a trace mineral that plays a role in antioxidant defenses as a component of glutathione peroxidase. Epidemiologic findings on the relation of selenium status to risk of heart disease are inconsistent. Therefore, the authors investigated prospectively the association between toenail selenium levels and risk of coronary heart disease (CHD) in a case-control study nested within the Health Professionals Follow-up Study. Between 1987 and 1992, 470 CHD cases were newly diagnosed. A control matched to each case on age, smoking status, and date of toenail return was chosen. Toenail selenium levels analyzed by neutron activation were not associated with risk of total CHD after adjustment for age and smoking and other CHD risk factors (highest quintile vs. lowest: odds ratio (OR) = 0.86, 95% confidence interval (CI): 0.55, 1.32; p-trend = 0.75). Selenium level was inversely associated with risk of nonfatal myocardial infarction for extreme quintiles (OR = 0.54, 95% CI: 0.31, 0.93; p-trend = 0.07), was less so for fatal CHD (OR = 0.79, 95% CI: 0.39, 1.60; p-trend = 0.61), and was directly associated with coronary revascularization procedures (OR = 2.38, 95% CI: 1.11, 5.09; p-trend = 0.02). Although these findings suggest no overall relation between selenium status and CHD, a specific protective role for myocardial infarction cannot be excluded.
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PMID:Prospective study of selenium levels in toenails and risk of coronary heart disease in men. 1458 63


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