Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Selenium is of fundamental importance to human health. It is an essential component of several major metabolic pathways, including thyroid hormone metabolism, antioxidant defence systems, and immune function. The decline in blood selenium concentration in the UK and other European Union countries has therefore several potential public health implications, particularly in relation to the chronic disease prevalence of the Western world such as cancer and cardiovascular disease. Ten years have elapsed since recommended dietary intakes of selenium were introduced on the basis of blood glutathione peroxidase activity. Since then 30 new selenoproteins have been identified, of which 15 have been purified to allow characterisation of their biological function. The long term health implications in relation to declining selenium intakes have not yet been thoroughly examined, yet the implicit importance of selenium to human health is recognised universally. Selenium is incorporated as selenocysteine at the active site of a wide range of selenoproteins. The four glutathione peroxidase enzymes (classical GPx1, gastrointestinal GPx2, plasma GPx3, phospholipid hydroperoxide GPx4)) which represent a major class of functionally important selenoproteins, were the first to be characterised. Thioredoxin reductase (TR) is a recently identified seleno-cysteine containing enzyme which catalyzes the NADPH dependent reduction of thioredoxin and therefore plays a regulatory role in its metabolic activity. Approximately 60% of Se in plasma is incorporated in selenoprotein P which contains 10 Se atoms per molecule as selenocysteine, and may serve as a transport protein for Se. However, selenoprotein-P is also expressed in many tissues which suggests that although it may facilitate whole body Se distribution, this may not be its sole function. A second major class of selenoproteins are the iodothyronine deiodinase enzymes which catalyse the 5'5-mono-deiodination of the prohormone thyroxine (T4) to the active thyroid hormone 3,3'5-triiodothyronine (T3). Sperm capsule selenoprotein is localised in the mid-peice portion of spermatozoa where it stabilises the integrity of the sperm flagella. Se intake effects tissue concentrations of selenoprotein W which is reported to be necessary for muscle metabolism. It is of great concern that the health implications of the decline in Se status in the UK over the past two decades have not been systematically investigated. It is well recognised that dietary selenium is important for a healthy immune response. There is also evidence that Se has a protective effect against some forms of cancer; that it may enhance male fertility; decrease cardiovascular disease mortality, and regulate the inflammatory mediators in asthma. The potential influence of Se on these chronic diseases within the European population are important considerations when assessing Se requirement.
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PMID:Selenium, selenoproteins and human health: a review. 1168 52

In order to investigate the relations of iodine deficiency and/or goiter with selenium (Se) and antioxidant enzyme (AOE) status, we determined the relevant parameters of goitrous high school children living in an endemic goiter area of Turkey. Subjects were selected by a simple random sampling technique after screening the whole population of the high schools of two towns by neck palpation. The results of the goitrous group (n = 48, aged 15-18 yr) were compared with those of nongoitrous control children (n = 49) from the same populations, and with an outside control group (n = 24) from a lower-goiter-prevalence area. The overall prevalence of goiter was 39.6% in the high school population of the area. Activities of erythrocyte AOE (glutathion peroxidase, catalase, and superoxide dismutase) and concentrations of plasma and erythrocyte Se and urinary iodine were found to be significantly lower in goitrous children than both in-region and out-region of the control groups. When the whole study group was reclassified according to the severity of iodine deficiency, it was found that the AOE and Se status of those control children without goiter but with high iodine deficiency was significantly higher than goitrous children, although they did not differ from nondeficient control group. This might be the result of the possibility that goitrous children are exposed of oxidative stress, which may introduce alterations to the antioxidant defense system and/or the antioxidant status is relatively lower in goitrous children than those children who are highly iodine-deficient but did not develop goiter. The results of this study seem to support the view that the risk of goiter development may be higher in highly iodine-deficient children with lower enzymatic antioxidant and Se status.
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PMID:Status of selenium and antioxidant enzymes of goitrous children is lower than healthy controls and nongoitrous children with high iodine deficiency. 1169 77

Reactive oxygen species (ROS) are known mediators of intracellular signaling cascades. Excessive production of ROS may, however, lead to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis. A balance between oxidant and antioxidant intracellular systems is hence vital for cell function, regulation, and adaptation to diverse growth conditions. Thioredoxin reductase (TrxR) in conjunction with thioredoxin (Trx) is a ubiquitous oxidoreductase system with antioxidant and redox regulatory roles. In mammals, extracellular forms of Trx also have cytokine-like effects. Mammalian TrxR has a highly reactive active site selenocysteine residue resulting in a profound reductive capacity, reducing several substrates in addition to Trx. Due to the reactivity of TrxR, the enzyme is inhibited by many clinically used electrophilic compounds including nitrosoureas, aurothioglucose, platinum compounds, and retinoic acid derivatives. The properties of TrxR in combination with the functions of Trx position this system at the core of cellular thiol redox control and antioxidant defense. In this review, we focus on the reactions of the Trx system with ROS molecules and different cellular antioxidant enzymes. We summarize the TrxR-catalyzed regeneration of several antioxidant compounds, including ascorbic acid (vitamin C), selenium-containing substances, lipoic acid, and ubiquinone (Q10). We also discuss the general cellular effects of TrxR inhibition. Dinitrohalobenzenes constitute a unique class of immunostimulatory TrxR inhibitors and we consider the immunomodulatory effects of dinitrohalobenzene compounds in view of their reactions with the Trx system.
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PMID:Reactive oxygen species, antioxidants, and the mammalian thioredoxin system. 1172 1

Evidence is accumulating indicating the importance of antioxidant enzyme activity measurements in eco-toxicological studies, as they may constitute markers for exposure to a large variety of pollutants. Variation of antioxidant enzymes, superoxide dismutase (SOD) and glutathione S-transferases (GST) and the effect of heavy metals and selenium exposure on these enzymes were investigated in the livers of Iberian endemic minnows (Leuciscus alburnoides complex) captured in a copper (Cu) mining area. Higher hepatic levels of copper and selenium were always observed in fish captured at the polluted site relative to the reference area population, reflecting the environmental monitoring results. A seasonal fluctuation in zinc and selenium levels for both populations was also observed which could be related to gonad maturation. The activity of SOD did not show significant regional alterations, but a seasonal variation occurred presumably associated with the Leuciscus life cycle. The GST activity was higher in the fish population from the polluted area (except in spring) and GST variability was associated with selenium and copper levels when both regions were compared. The increased GST activity was probably a metabolic adaptation to the continuous exposure to higher levels of those elements.
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PMID:Response of antioxidant enzymes in freshwater fish populations (Leuciscus alburnoides complex) to inorganic pollutants exposure. 1176 63

Exposure of living organisms to reactive oxygen species (ROS), notably oxygen free radicals and hydrogen peroxide is closely linked to the very fact of aerobic life. Oxidants, however, are not always detrimental for cell survival, indeed moderate concentrations of ROS serve as signaling molecules. To maintain this level, cells have evolved an antioxidant defense system. Disruption of this balance leads either to oxidative or reductive stress. Down syndrome (DS) is a genetic disorder associated with oxidative stress. Overexpression of superoxide dismutase-1 (SOD-1) as a result of gene loading is suggested to be responsible for this phenomenon. To examine this view, we investigated the expression of thirteen different proteins involved in the cellular antioxidant defense system in brains of control and DS fetuses by two-dimensional electrophoresis (2-DE) coupled with matrix-assisted laser desorption/ionization mass spectroscopy (MALDI-MS). No detectable change was found in expression of SOD-1, catalase, phospholipid hydroperoxide glutathione peroxidase, glutathione reductase, antioxidant enzyme AOE372, thioredoxin-like protein and selenium binding protein between control and DS fetuses. By contrast, a significant reduction was observed in levels of glutathione synthetase (P < 0.01), glutathione-S-transferase mu2 (P < 0.01), glutathione-S-transferase p (P < 0.05), antioxidant protein 2 (P < 0.05), thioredoxin peroxidase-I (P < 0.05) and thioredoxin peroxidase-II (P < 0.01) in DS compared with controls. The data suggest that oxidative stress in fetal DS does not result from overexpression of SOD-1 protein, rather oxidative stress appears to be the consequence of low levels of reducing agents and enzymes involved in removal of hydrogen peroxide.
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PMID:Antioxidant proteins in fetal brain: superoxide dismutase-1 (SOD-1) protein is not overexpressed in fetal Down syndrome. 1177 62

Previously, we found that macrophage colony-stimulating factor (M-CSF) could reduce tert-butyl hydroperoxide (tbOOH)-induced oxidative injury in monocytes/macrophages. In order to find the mechanism by which M-CSF achieves this, we investigate the effect of M-CSF on the antioxidant system in murine macrophage RAW264.7 cells, using L929 cell-conditioned medium (L929-CM) as the source of M-CSF. The results show that L929-CM increased selenium-dependent glutathione peroxidase, non-selenium-dependent glutathione peroxidase, and catalase activities; and it increased reduced glutathione (GSH) but decreased lipoperoxide content in RAW264.7 cells. L929-CM-treated cells maintained their antioxidant capacity (including antioxidant enzyme activities and GSH content) when challenged with tbOOH. We conclude that M-CSF from L929-CM reduces oxidative injury in RAW264.7 cells by increasing antioxidant enzyme activity and improving redox status.
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PMID:Effect of L929 cell-conditioned medium on antioxidant capacity in RAW264.7 cells. 1178 96

A pure selenium deficiency is harmful to the heart and causes a fatal dilated congestive cardiomyopathy in animals (white muscle disease) and in man (Keshan disease). Both of these syndromes are selenium-responsive. A deficiency of the micronutrient has also been reported in patients with Friedreich's ataxia and there are histological similarities between Friedreich's cardiomyopathy and Keshan disease. A low selenium status results in reduced selenium-dependent glutathione peroxidase activity. This essential antioxidant enzyme protects membrances from oxidative deterioration, a function it shares in common with vitamin E. As iron-induced mitochondrial lipid peroxidation is central to the pathology of Friedreich's ataxia, the administration of selenium supplements should normalize the antioxidant activity of myocardial glutathione peroxidase and slow the progression of the life-shortening cardiomyopathy associated with this illness.
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PMID:Rationale for clinical trials of selenium as an antioxidant for the treatment of the cardiomyopathy of Friedreich's ataxia. 1181 88

Heart failure due to chronic iron overload is a leading cause of cardiovascular mortality in the second and third decades of life worldwide, but its mechanism is not known. Deficiencies of selenium have been shown to result in damage to the myocardium and to the development of various cardiomyopathies. In the current investigation, the dose-dependent effects of chronic iron toxicosis on heart tissue concentrations of selenium and the protective antioxidant enzyme glutathione peroxidase (GPx) were investigated in a murine model of iron-overload cardiomyopathy (n = 20). Significant dose-dependent decreases in heart tissue selenium concentrations (r = -0.95, p < 0.001) and selenium-dependent GPx activity (r = -0.93, p < 0.001) were observed in chronically iron-loaded mice in comparison with placebo controls. These results suggest that dietary supplementation with selenium may be beneficial in the clinical management of disorders of iron metabolism.
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PMID:Decreasing effects of iron toxicosis on selenium and glutathione peroxidase activity. 1185 44

The levels of some organochlorine pesticides (OCP)s (hexachlorobenzene, HCB, alpha-hexachlorocyclohexane, alpha-HCH, beta-HCH, gamma-HCH, heptachlorepoxide, HE, bis (4-chlorophenyl)-1,1-dichloroethene, p.p'DDE, bis (4-chlorophenyl)-1,1,1-trichloroethane, p.p' DDT and total DDT (E-DDT) and antioxidant enzyme activities namely Cu, Zn superoxide dismutase (SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px), total glutathione peroxidase (T-GSH-Px), selenium independent glutathione peroxidase (GSH-Px II), glutathione reductase (GRd), level of reduced glutathione (GSH) and lipid peroxidation (LP), glutathione S-transferase (GST) activity toward several substrates including 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), 1,2-epoxy-3-(p-nitrophenoxy)-propane (ENPP) were measured in tumor and surrounding tumor free tissues of 24 female breast cancer patients and was evaluated whether there exist any association between the levels of OCPs and antioxidants. The mean levels of GSH, alpha-BHC, gamma-BHC and HE, and activities of SOD, Se-GSH-Px, T-GSH-Px, GSH-Px II,GRd, GST CDNB, and GST DCNB were significantly higher in tumors than in controls. In tumors, significant correlations were noted between: SOD and y-BHC; Se-GSH-Px and gamma-BHC; T-GSH-Px and gamma-BHC; GSH-Px II and alpha-BHC, gamma-BHC; GSH and alpha-BHC, gamma-BHC, HE; GRd and alpha-BHC; CDNB GST and alpha-BHC, gamma-BHC. These results show that free-radical mediated oxidative stress is, at least partly, associated with some of these OCP residues in human breast tumors.
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PMID:The organochlorine pesticide residues and antioxidant enzyme activities in human breast tumors: is there any association? 1203 8

Selenium is a trace element of tremendous importance in human health. It is a constituent of the antioxidant enzyme. Glutathione peroxidase and therefore is vital to antioxidant defense. Several diseases of the neonate have been shown to be caused at least in part by oxygen free radicals. These include bronchopulmonary dysplasia retinopathy of prematurity necrotising enterocolitis patient ductus arteriosus and neuronal injury of hypoxic ischemic encephalopathy. Good selenium nutrition is therefore of key importance to antioxidant defense in the neonate. The communique reviews the important role that selenium might play in neonatal health & disease.
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PMID:Selenium in the neonate. 1206 82


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