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)

In the present study, we tested the hypothesis that Bos taurus taurus bulls have greater reactive oxygen species (ROS) and lower activity of antioxidant enzymes in their semen than Bos taurus indicus bulls. Sixteen Simmental bulls (B. t. taurus) and 11 Nelore bulls (B. t. indicus) were managed extensively in a tropical environment. Semen was collected twice annually (summer and winter) for 2 consecutive years. Simmental bulls had significantly higher percentages of major sperm defects during the summer than the winter (20.3+/-3.1% versus 12.2+/-2.4%, respectively; mean+/-S.E.M.). There was an interaction of breed and season for minor sperm defects (P=0.037; highest in Nelore bulls in the summer) and an effect of season on total defects (P=0.066; higher in summer). To evaluate oxidative damage, malondialdehyde (lipid-peroxidation metabolite) concentrations were indirectly measured by semen concentrations of thiobarbituric acid reactive substances (TBARS); these were higher in summer than in winter (728.1+/-79.3ng/mL versus 423.8+/-72.6ng/mL, respectively; P=0.01). Glutathione peroxidase/redutase (GPx) activity in semen was higher in Simmental versus Nelore bulls (741.6+/-62.1 versus 510.2+/-62.8; P<0.01). However, superoxide dismutase (SOD), another antioxidant enzyme, was not significantly affected by breed or season. There were correlations between TBARS and sperm primary defects during the summer for both Simmental and Nelore bulls (r=0.59, P=0.021 and r=0.40, P=0.034, respectively), and between SOD and primary defects during summer for Simmental bulls only (r=-0.51, P=0.041). In conclusion, there was a higher level of lipid peroxidation (ROS) in semen of Simmental versus Nelore bulls; apparently the higher GPx activity in Simmental bulls was insufficient to avoid damage that occurred concurrent with increased ROS production during the summer.
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PMID:Seasonal variation in semen quality in Bos indicus and Bos taurus bulls raised under tropical conditions. 1652 2

Oxidative stress plays an important role in the structural and functional abnormalities of diabetic heart. Glutathione peroxidase (GSHPx) is a critical antioxidant enzyme that removes H(2)O(2) in both the cytosol and mitochondia. We hypothesized that the overexpression of GSHPx gene could attenuate left ventricular (LV) remodeling in diabetes mellitus (DM). We induced DM by injection of streptozotocin (160 mg/kg ip) in male GSHPx transgenic mice (TG+DM) and nontransgenic wildtype littermates (WT+DM). GSHPx activity was higher in the hearts of TG mice compared with WT mice, with no significant changes in other antioxidant enzymes. LV thiobarbituric acid-reactive substances measured in TG+DM at 8 wk were significantly lower than those in WT+DM (58 +/- 3 vs. 71 +/- 5 nmol/g, P < 0.05). Heart rate and aortic blood pressure were comparable between groups. Systolic function was preserved normal in WT+DM and TG+DM mice. In contrast, diastolic function was impaired in WT+DM and was improved in TG+DM as assessed by the deceleration time of peak velocity of transmitral diastolic flow and the time needed for relaxation of 50% maximal LV pressure to baseline value (tau; 13.5 +/- 1.2 vs. 8.9 +/- 0.7 ms, P < 0.01). The TG+DM values were comparable with those of WT+Control (tau; 7.8 +/- 0.2 ms). Improvement of LV diastolic function was accompanied by the attenuation of myocyte hypertrophy, interstitial fibrosis, and apoptosis. Overexpression of GSHPx gene ameliorated LV remodeling and diastolic dysfunction in DM. Therapies designed to interfere with oxidative stress might be beneficial to prevent cardiac abnormalities in DM.
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PMID:Overexpression of glutathione peroxidase attenuates myocardial remodeling and preserves diastolic function in diabetic heart. 1684 17

The aim was to study the effects of a scuba diving session on the lymphocyte antioxidant system, NO synthesis, the capability to produce reactive oxygen species and the antioxidant response in neutrophils. For that purpose seven male divers performed an immersion at a depth of 40 m for 25 min. The same parameters were measured after an hyperbaric oxygen (HBO) treatment at resting conditions in a hyperbaric chamber. Lymphocyte H2O2 production rose after diving and after HBO treatment. Glutathione peroxidase (GPx) and catalase activities increased after diving in lymphocytes, while after HBO exposure only increased GPx activity. Lymphocyte HO-1 mRNA expression increased after diving and after HBO exposure, while iNOS levels and nitrite levels significantly increased after diving. The hyperoxia associated to scuba diving leads to a condition of oxidative stress with increased lymphocyte H2O2 production, HO-1 expression, NO synthesis and antioxidant enzyme adaptations in order to avoid oxidative damage.
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PMID:Scuba diving enhances endogenous antioxidant defenses in lymphocytes and neutrophils. 1736 55

Mildly elevated homocysteine levels (Hcy) increase the risk for atherothrombotic vascular disease in the coronary, cerebrovascular, and peripheral arterial circulations. The molecular mechanisms responsible for decreased bioavailability of endothelium-derived nitric oxide (NO) by Hcy involve an increase of vascular oxidant stress and inhibition of important antioxidant capacity. Glutathione peroxidase-1 (GPx-1), a selenocysteine-containing antioxidant enzyme, may be a key target of Hcy's deleterious actions, and several experimental and clinical studies have demonstrated a complex relationship between plasma total homocysteine (tHcy), GPx-1, and endothelial dysfunction. Hcy may promote endothelial dysfunction, in part by decreasing GPx-1 expression; however, there is evidence to suggest that overexpression of GPx-1 can compensate for these effects. This review summarizes the current knowledge of the metabolism of Hcy, the effects of hyperhomocysteinemia observed in in vitro and in vivo models that lead to endothelial dysfunction and the possible mechanisms for these actions, and the role of GPx-1 in the pathogenesis of Hcy-induced cardiovascular disease (CVD).
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PMID:Homocysteine and glutathione peroxidase-1. 1782 68

We studied the antioxidant enzyme response of the gastropoda Bittium reticulatum feeding the toxic alga Caulerpa taxifolia, and also the effects of intense herbivorism on caulerpenyne production and on the antioxidant response of C. taxifolia. B. reticulatum were maintained in two separated aquariums containing Posidonia oceanica or C. taxifolia. Glutathione peroxidase, glutathione reductase and glutathione S-transferase activities were significantly higher in B. reticulatum living in presence of C. taxifolia with respect to animals living in P. oceanica aquarium. Malondialdehyde levels in B. reticulatum showed similar values in both environments. Caulerpenyne levels were significantly higher in C. taxifolia fronds after herbivore exposure. C. taxifolia activities of catalase and glutathione reductase significantly increased in presence of B. reticulatum. B. reticulatum exposed to caulerpenyne evidenced antioxidant enzyme adaptations to prevent oxidative damage. The presence of B. reticulatum in the aquarium induces a protective adaptation in C. taxifolia in order to reduce the herbivorism.
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PMID:Reciprocal effects of caulerpenyne and intense herbivorism on the antioxidant response of Bittium reticulatum and Caulerpa taxifolia. 1823 33

The aim of the study was to determine the selenium (Se) requirement of guinea pigs as a species unable to synthesize ascorbic acid. Forty-nine male guinea pigs (average weight 208 +/- 3.5 g) were divided into an initial status group and six experimental groups. The animals received a Se deficient Torula yeast based basal diet (<0.02 mg Se and 26 mg alpha-tocopherol/kg) or a Se addition of 0.05, 0.10, 0.15, 0.20 and 0.25 mg/kg diet as sodium selenate for 10 weeks. There was no significant difference in weight gain (final weight 643 +/- 21 g) between the groups and no clinical symptoms of Se deficiency occurred. With the exception of the testes, there was an increasing Se concentration in liver, plasma and haemolysate dependent on supplementation level. Glutathione peroxidase was determined in the plasma and Se dependent glutathione peroxidase (GPx1) in haemolysate, liver, kidney, heart and lung. Thioredoxin reductase (TR) activity was measured in liver, kidney and heart and deiodinase activity in the liver. A phospholipid hydroperoxide reducing activity with Se influence was determined in liver, kidney, heart, testes and brain. With the exception of GPx1 activity in heart and haemolysate and TR activity in the kidney, all enzymes already reached their maximal activity at 0.05 mg Se/kg diet. The activities of GPx1 and TR were used as parameters for broken line analysis and a Se requirement of 0.080 mg Se/kg diet was derived as sufficient for growing guinea pigs adequately supplied with vitamin E.
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PMID:Estimation of the selenium requirement of growing guinea pigs (Cavia porcellus). 1866 58

Glutathione peroxidase (GPx-1) is regarded as one of the mammalian cell's main antioxidant enzymes inactivating hydrogen peroxide and protecting against oxidative stress. Using control, Parkinson's disease (PD), and dementia with Lewy bodies tissue (DLB) we have shown that GPx-1 is a 21-kD protein under reducing conditions in all tissues examined but is not in high abundance in human brain. Using immunohistochemistry we have mapped the cellular distribution of GPx-1 and have shown it to be in highest levels in microglia and with lower levels in neurons. Only a trace amount was detectable in astrocytes using immunofluorescence and GPx-1 was not detectable in oligodendrocytes. GPx-1 positive microglia were hypertrophied and more abundant in PD and DLB tissues and were seen to be making multiple contacts with neurons. In some cases neurons containing Lewy bodies were surrounded by microglia. Unstructured Lewy bodies were enveloped with a layer of GPx-1 that was partially colocalized with alpha-synuclein whereas concentric Lewy bodies had discrete deposits of GPx-1 around the periphery which appeared to be involved in the degradation of the Lewy bodies. These results suggest that abnormal alpha-synuclein as found in Lewy bodies produce hydrogen peroxide and these neurons are capable of directing antioxidant enzymes to regions of oxidative stress. These results also suggest that GPx-1 positive microglia are involved in neuroprotection in PD and DLB and that GPx-1 is an important antioxidant enzyme in neuronal defences.
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PMID:Cellular glutathione peroxidase in human brain: cellular distribution, and its potential role in the degradation of Lewy bodies in Parkinson's disease and dementia with Lewy bodies. 1885 69

Free radicals that induced lipid peroxidation and DNA damage have been implicated in many diseases including cancer. Cellular antioxidant defense plays an important role in neoplastic disease to counteract oxidative damage. This study aims to investigate the status of oxidative damage by measuring plasma malondialdehyde (MDA) level and urinary 8-hydroxydeoxyguanosine (8-OHdG), and the level of antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase in patients with cervical intraepithelial neoplasia (CIN) and squamous cell carcinoma (SCC) of the cervix. Urinary 8-OHdG was measured by an enzyme-linked immunosorbent assay kit. MDA and antioxidant enzyme activities were determined by high-performance liquid chromatography and spectrophotometry, respectively. Eighty patients with CIN and SCC of the cervix were recruited and compared with normal controls. Urinary 8-OHdG/creatinine ratio did not show any significant changes in any disease status studied as compared with controls (P=0.803). Plasma MDA was found to be increased in CIN and SCC patients when compared with controls (P=0.002). Glutathione peroxidase activity was increased (P=0.0001) whereas superoxide dismutase and catalase activity was decreased (P=0.019 and 0.0001, respectively) in both CIN and SCC patients when compared with controls. Urinary 8-OHdG may not be a good marker for enhanced oxidative stress in cervical cancer. Oxidative damage as demonstrated by the level of MDA is markedly increased in CIN and SCC patients with changes of enzymatic antioxidants observed.
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PMID:Oxidative damage and antioxidant status in patients with cervical intraepithelial neoplasia and carcinoma of the cervix. 1894 77

Glutathione peroxidase (GPX) is an important antioxidant enzyme, which plays an important role in scavenging reactive oxygen species. To obtain humanized GPX catalytic antibodies, the phage displayed human antibody library on the surface of the filamentous bacteriophage was used to select novel antibodies by repetitive screening. Phage antibodies B8, H6 and C1 with the GSH-binding site were obtained from the library by enzyme-linked immunosorbent assay (ELISA) analysis with four rounds of selection against three haptens, S-2,4-dinitrophenyl t-butyl ester [GSH-S-DNP-Bu (B)], S-2,4-dinitrophenyl t-hexyl ester [GSH-S-DNP-He (H)] and S-2,4-dinitrophenyl cycle-hexyl ester [GSH-S-DNP-cHe (C)], and characterized using surface plasmon resonance (SPR) biosensor. The gold layer was modified by dithiodiglycolic acid (DDA) and three haptens were easily attached to DDA by self-assembling to form a biosensor membrane. The membrane bounds specifically corresponding antibodies. The kinetic process of the reaction between phage antibodies and their haptens was studied by SPR biosensor. In order to improve selectivity, chemical modification was used to incorporate directly catalytic group selenocysteine (Sec) into selected phage clone B8, H6 and C1 to form Se-B8, Se-H6 and Se-C1, respectively. The GPX activities of Se-B8, Se-H6 and Se-C1 were found to be 3000, 2000 and 700units/mumol, respectively. Compared with conventional ELISA analysis, the proposed method based on SPR biosensor is much more rapid and simpler.
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PMID:Selection of phage antibodies with GPX activity by combination of phage displayed antibody library with chemical modification and their characterization using a surface plasmon resonance biosensor. 1896 79

The aim of this study is to evaluate the erythrocyte lipid peroxidation and antioxidant enzyme levels in patients with newly diagnosed idiopathic epilepsy before treatment and in patients treated with valproic acid for idiopathic epilepsy. Twenty-four patients with newly diagnosed idiopathic epilepsy, 24 patients treated with valproic acid for idiopathic epilepsy and 21 healthy children were included in the study. Malondialdehyde as an indicator of lipid peroxidation and antioxidants enzymes including superoxide dismutase and glutathione peroxidase were measured in the erythrocytes. The levels of malondialdehyde were significantly lower and activity of superoxide dismutase was insignificantly higher in patients with newly diagnosed epilepsy. Glutathione peroxidase levels did not differ between the groups. During treatment with valproic acid, lipid peroxidation increased but did not reach pathological levels. There was a positive correlation between superoxide dismutase activity and duration of valproic acid treatment. In conclusion, oxidant-antioxidant status is impaired in patients with primary idiopathic epilepsy and scavenger systems are activated to decrease lipid peroxidation. Valproic acid which is frequently used in childhood epilepsy may modify the balance between oxidant and antioxidant systems.
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PMID:Effects of epilepsy and valproic acid on oxidant status in children with idiopathic epilepsy. 1926 43


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