Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.9 (glutathione peroxidase)
22,002 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differentiation-arrested monolayer lung cell cultures were developed from day 18, 20, and 22 rat fetuses and 3-day-old neonatal rats. These cultures were examined for antioxidant enzyme activity, and the values obtained were compared with previously reported in vivo activity. All cultures were catalase deficient, and activity could be restored by the addition of 0.25 microM Fe(NO3)3 X 9H2O to the culture medium. The other measured antioxidant enzymes--copper-zinc and manganese superoxide dismutase, glutathione peroxidase, and glucose 6-phosphate dehydrogenase-demonstrate gestation-dependent increases of activity in vivo that were not evident in vitro, supporting the concept of a circulating "maturation factor" during fetal life. When cultures from fetal days 20 and 22 and from neonatal day 3 lungs were challenged with 50% oxygen in the presence of serum, antioxidant enzyme activities were unchanged, and there was no evidence of cell damage as assessed by release of lactate dehydrogenase. In the absence of serum, however, fetal day 20 (but not fetal day 22 or neonatal day 3) lung cells showed evidence of cell damage and increased antioxidant enzyme activities. It is concluded that cultured immature fetal cells are more susceptible to oxygen toxicity than those derived from mature fetal or neonatal animals. This increased susceptibility cannot be explained on the basis of the reduced antioxidant enzyme activity observed in vivo.
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PMID:Differentiation-arrested rat fetal lung in primary monolayer cell culture. III. Antioxidant enzyme activity. 674 12

In order to assess the reference values for selenium nutritional status, adequate indicators (selenium concentration and glutathione peroxidase activity) were determined in whole blood and blood derivates of a healthy population (n = 287) from the province of Valencia, Spain. The reference population was selected by applying preestablished criteria. Selenium in whole blood and plasma was measured by graphite furnace atomic absorption spectrometry (GFAAS), with a deuterium correction, after addition of Pd/Mg(NO3)2 as the matrix modifier and appropriate dilution. Accuracy was checked by means of a reference material (Seronorm Trace Metals serum and whole blood). The population's reference intervals for selenium content at a 95% confidence level were: 53.03-108.96 and 66.71-119.4 mg/L for plasma and whole blood selenium concentration respectively. GPX activity was measured using a modification of the Paglia and Valentine method, and the reference intervals obtained ranged from 196 to 477 U/L in plasma, from 49 to 93 U/gHb in erythrocytes and from 52 to 96 U/gHb in whole blood. The only statistically significant differences detected between men and women are for to the GPX activity in whole blood. The results obtained are in the range of values found by others authors in healthy populations residing in different European countries.
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PMID:Selenium and glutathione peroxidase reference values in whole blood and plasma of a reference population living in Valencia, Spain. 902 73

There is a requirement for cellular defense against excessive peroxynitrite generation to protect against DNA strand breaks and mutations and against interference with protein tyrosine-based signaling and other protein functions due to formation of 3-nitrotyrosine. Here, we demonstrate a role of selenium-containing enzymes catalyzing peroxynitrite reduction using glutathione peroxidase (GPx) as an example. GPx protected against the oxidation of dihydrorhodamine 123 by peroxynitrite more effectively than ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), a selenoorganic compound exhibiting a high second-order rate constant for the reaction with peroxynitrite, 2 x 10(6) M-1 s-1. Carboxymethylation of selenocysteine in GPx by iodoacetate led to the loss of "classical" glutathione peroxidase activity but maintained protection against peroxynitrite-mediated oxidation. The maintenance of protection by GPx against peroxynitrite requires GSH as reductant. When peroxynitrite was infused to maintain a 0.2 microM steady-state concentration, GPx in the presence of GSH, but neither GPx nor GSH alone, effectively inhibited the hydroxylation of benzoate by peroxynitrite. Under these steady-state conditions peroxynitrite did not cause the loss of classical GPx activity. GPx, like selenomethionine, protected against protein 3-nitrotyrosine formation in human fibroblast lysates, shown in Western blots. The formation of nitrite rather than nitrate from peroxynitrite was enhanced by GPx or by selenomethionine. The results demonstrate a novel function of GPx and potentially of other selenoproteins containing selenocysteine or selenomethionine, in the GSH-dependent maintenance of a defense line against peroxynitrite-mediated oxidations, as a peroxynitrite reductase.
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PMID:Glutathione peroxidase protects against peroxynitrite-mediated oxidations. A new function for selenoproteins as peroxynitrite reductase. 934 26

The effects of bismuth nitrate (BN) on the lethal effect of and injury to bone marrow by gamma-irradiation were examined. Mice were given daily s.c. injections of BN for 2 days and were exposed to whole-body irradiation (137Cs; 8 grays) 24 hr after the second injection of BN. All mice exposed to gamma-irradiation without treatment with BN died within 30 days, but the lethal effect of gamma-irradiation was markedly reduced in mice given BN before irradiation. Irradiation (3 grays) significantly reduced the total number of leukocytes 1 day after irradiation but the number of leukocytes subsequently increased in both nontreated and BN-treated irradiated mice. However, the rate of recovery of the total number of leukocytes, as monitored from 5 days after irradiation, was significantly higher in BN-treated mice than in the nontreated mice. Reductions in the viability of hematopoietic stem cells (determined by monitoring the number of colony-forming units in the spleen) that were induced by gamma-irradiation (3 grays) were considerably diminished by the treatment of mice with BN before irradiation. BN significantly increased the concentration of metallothionein in the bone marrow cells of mice, but levels of other cellular antioxidants, such as catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase and glutathione, were unchanged. These results suggest that BN protects bone marrow cells against the toxic effects of gamma-irradiation by inducing the synthesis of metallothionein in the bone marrow. Metallothionein might play an important role in determining the sensitivity of animals to gamma-irradiation.
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PMID:Protective effect of bismuth nitrate against injury to the bone marrow by gamma-irradiation in mice: possible involvement of induction of metallothionein synthesis. 973 7

The metabolisms of reactive nitrogen and oxygen intermediates (RNI and ROI) in patients with cutaneous leishmaniasis (CL) were investigated and compared with those of healthy subjects. To determine RNI metabolism, nitrite plus nitrate concentrations were measured spectrophotometrically. Nitrite concentration in plasma was determined directly by the Griess method. Nitrate levels in plasma were measured after reduction into nitrite by using copper-cadmium-zinc. ROI metabolism was evaluated by measuring erythrocyte superoxide dismutase, catalase and glutathione peroxidase activities. Plasma nitrite plus nitrate levels and erythrocyte superoxide dismutase activity were higher in the patient group than healthy subjects (p<0.01). In contrast, erythrocyte catalase and glutathione peroxidase activities were lower (p<0.05, p<0.01, respectively). ROI metabolism was altered in relation to hydrogen peroxide elevation in patients with CL. These alterations in ROI enable nitric oxide (NO) to amplify its leishmanicidal effect. The determination of ROI and RNI in patients with CL may be a useful tool to evaluate effector mechanisms of NO and clinical manifestations.
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PMID:Reactive nitrogen and oxygen intermediates in patients with cutaneous leishmaniasis. 1022 24

The mechanism of oxidation or reduction using the electron method was investigated for (I) aniline; (II) nitrobenzene; (III) nitrate; (IV) sulphanilamide; (V) hydrogen peroxide; (VI) hydroxyl free radical; (VII) ferricyanide; (VIII) acetylphenylhydrazine; (IX) nitrite; (X) chlorate and (XI) hydroxylamine respectively. Substances (II), (III), (V), (VI), (VII), (IX), (X) and (XI) evolved as oxidants, with (II), nitrobenzene and (X), chlorate as the most powerful oxidants (number of moles of HbFe(2+)(haemoglobin) of 6 reacting with 1.0 mole of the substance). Substances (I), (IV) and (VII) evolved as reductants of equal reducing power (number of moles of HbFe(3+)(methaemoglobin) of 4 reacting with 1.0 mole of the substance). Using the following equations, the impact of oxidants and reductants on glutathione (GSH) peroxidase, glutathione (GSSC) reductase and NADHmetHb reductase respectively on methaemoglobinaemia generation was investigated. [Equation in text]. Redox potential change (DeltaE' (o)) of 1.77, -1.77 and 1.86 volt and free energy change (DeltaG(o)') of -81, 81 and -85.8 kcal/mol were calculated for GSH peroxidase, GSSG reductase and NADHmetHb reductase systems respectively. In sustained methaemoglobinaemia, these mechanisms predict low levels of NADHmetHb reductase and glutathione peroxidase respectively, but high levels of glutathione reductase in red blood cells on exposure to oxidants. The significance of these mechanisms was investigated in cord blood, neonatal, adult red blood cells and other biological systems. It was concluded that any reaction with a positive DeltaE(o)' and negative DeltaG(o)' with the Fe(3+): Fe(2+)couple will indicate methaemoglobin oxidizing power. The effects on red blood cells and white blood cells were manifested in the biochemical toxicology of nitroso (PhN = 0), arylamine glucuronide (PhNHG) and arene imine respectively.
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PMID:Theoretical mechanistic basis of oxidants of methaemoglobin formation. 1079 Jul 68

Oxidants have been shown to be involved in alcohol-induced liver injury. Moreover, 2-phenyl-1,2-benzisoselenazole-3(2H)-one (ebselen), an organoselenium compound and glutathione peroxidase mimic, decreases oxidative stress and protects against stroke clinically. This study was designed to test the hypothesis that ebselen protects against early alcohol-induced liver injury in rats. Male Wistar rats were fed high-fat liquid diets with or without ethanol (10-16 g/kg/d) continuously for up to 4 weeks using the intragastric enteral feeding protocol developed by Tsukamoto and French. Ebselen (50 mg/kg twice daily, intragastrically) or vehicle (1% tylose) was administered throughout the experiment. Mean urine ethanol concentrations were not significantly different between treatment groups, and ebselen did not affect body weight gains or cyclic patterns of ethanol concentrations in urine. After 4 weeks, serum ALT levels were increased significantly about 4-fold over control values (37 +/- 5 IU/l) by enteral ethanol (112 +/- 7 IU/l); ebselen blunted this increase significantly (61 +/- 8 IU/l). Enteral ethanol also caused severe fatty accumulation, mild inflammation, and necrosis in the liver (pathology score: 4.3 +/- 0.3). In contrast, these pathological changes were blunted significantly by ebselen (pathology score: 2.5 +/- 0.4). While there were no significant effects of either ethanol or ebselen on glutathione peroxidase activity in serum or liver tissue, ebselen blocked the increase in serum nitrate/nitrite caused by ethanol. Furthermore, ethanol increased the activity of NF-kappaB over 5-fold, the number of infiltrating neutrophils 4-fold, and the accumulation of 4-hydroxynonenal over 5-fold. Ebselen blunted all of these effects significantly. These results indicate that ebselen prevents early alcohol-induced liver injury, most likely by preventing oxidative stress, which decreases inflammation.
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PMID:Ebselen prevents early alcohol-induced liver injury in rats. 1118 96

In accordance with the present state of scientific knowledge, the excessive production of free radicals in the organism, and the imbalance between the concentrations of these and the antioxidant defenses may be related to processes such as aging and several diseases. The aging process has been described by various theories. In particular, the free radical theory of aging has received widespread attention which proposes that deleterious actions of free radicals are responsible for the functional deterioration associated with aging. Although, the relationship between lipid peroxidation and aging have been investigated extensively, the studies have produced conflicting results. To investigate the correlation between the oxidative stress and aging, we have determined the levels of lipid peroxidation expressed as thiobarbituric acid reactive substances (TBARS; MDA) and conjugated dien; oxidative protein damage as indicated by carbonyl content and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in a sample of 100 healthy men and women ranging in age from 20 to 70years. In addition, vitamin E, C levels, reduced glutathione and sulphydryl content were determined. The oxidation end product of nitric oxide (nitrate) was also studied to investigate any role of nitrogen radicals in aging. Our data show that there is an age related increase in lipid peroxidation expressed as MDA and oxidative protein damage as indicated by carbonyl content. Aging is not linked to a decline in antioxidant enzymes except GPx. Our data suggests that the level of oxidative stress increase cannot entirely be attributed to a decrease in the activities of antioxidant defense system and probably various factors may contribute to this process.
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PMID:Alterations of antioxidant enzymes and oxidative stress markers in aging. 1122 37

The present study was designed to evaluate the possible protective effect of quercetin, coenzyme Q10 (CoQ10), or L-canavanine treatments against endotoxin-induced shock in rat brain. Shock was induced by i.p. injection of 10 mg x kg(-1)of lipopolysaccharide (LPS) and was biochemically manifested 2 h after injection as an increase in brain malondialdehyde (MDA), total nitrite/nitrate (NO(x)), glutathione peroxidase (GSHPx), and blood lactate level/activity. On the other hand, endotoxemia resulted in reduced brain glutathione (GSH) and phospholipids' content as well as the serum sulfhydryl groups' (SH-group) value. Pretreatment with quercetin (200 mg x kg(-1)per os) 2 h before LPS injection diminished the shock-induced increases in brain MDA, and NO(x)levels while elevating the reduced brain phospholipids' and serum SH groups' content. CoQ10 administered at a dose of 200 mg x kg(-1)per os for 7 days prior to shock induction, reduced the elevated levels of brain MDA, NO(x), and GSHPx level/activity due to redundancy. The same treatment caused a 3-fold increase in the reduced brain GSH level and normalized the depressed phospholipids' content. Treatment of animals with L-canavanine (50 mg x kg(-1)i.p.) simultaneously with LPS injection, reduced the elevated level of blood lactate. Brain superoxide dismutase (SOD) level was neither affected by endotoxin nor by different treatments. In conclusion, this study indicates that SOD may not reflect the level of peroxidation and points to the value of quercetin, CoQ10, and L-canavanine in ameliorating the oxidative status of brain during the early phase of endotoxic shock.
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PMID:Quercetin, coenzyme Q10, and L-canavanine as protective agents against lipid peroxidation and nitric oxide generation in endotoxin-induced shock in rat brain. 1140 18

It is known that oxidative stress can be able to induce cytotoxicity of blood cells, stimulate release of inflammatory cytokines, and induce the production of growth factors. The aim of this study was to investigate oxidative stress and endothelial dysfunction in patients with asymptomatic carotid artery disease and healthy controls. Native low-density lipoproteins, oxidised low-density lipoproteins, malondialdehyde, nitrates, glutathione peroxidase activity and endothelin-1 were determined in patients without severe (range between 30% and 50%) carotid artery stenosis. Native low-density lipoproteins, oxidized low-density lipoproteins, malondialdehyde, glutathione peroxydase, and endothelin-1 concentrations were higher in patients than in health controls (P<0.001). No difference was observed in nitrate values (P<0.8). Our results revealed oxidative stress in patients without severe carotid artery stenosis and clinical symptoms. This was shown by the elevated malondialdehyde and oxidized low-density lipoprotein levels.
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PMID:Oxidative stress and endothelial damage in patients with asymptomatic carotid atherosclerosis. 1146 6


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