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)

Postprandial lipaemia is known to cause endothelial dysfunction, but its underlying mechanism is still under debate. The present study was undertaken to investigate the effects of postprandial lipaemia on endothelial dysfunction and oxidative stress. We measured plasma glutathione peroxidase (GSH-Px), an antioxidant enzyme, and the urinary excretion of 8-epi-prostaglandin F2alpha (8-PGF2alpha), a free radical-catalysed product from the oxidative modification of arachidonic acid, in 16 healthy subjects (mean age, 30 +/- 5 years) without major coronary risk factors. Plasma high-sensitive C-reactive protein, soluble intercellular cell-adhesion molecule-1 and vascular cell-adhesion molecule-1 were also measured. High-resolution ultrasound was used to assess the flow-mediated vasodilatation (FMD) of the brachial artery. Blood and urine samples were collected before and 2, 4 and 6 h after a standard high-fat meal (3677 J, containing 50 g of fat). Serum triacylglycerol (triglyceride) increased and FMD decreased significantly after a high-fat meal. Plasma GSH-Px significantly decreased from 27.2 +/- 12.3 microg/ml to 25.7 +/- 11.8 microg/ml (P=0.022) 2 h after the meal, and urinary excretion of 8-PGF2alpha significantly increased from 1286 +/- 1401 pg/mg of creatinine to 2197 +/- 1343 pg/mg of creatinine (P=0.014) at 4 h after the meal. However, there were no significant changes in the levels of high-sensitive C-reactive protein and adhesion molecules after a high-fat meal. In conclusion, endothelial dysfunction was observed after consuming a high-fat meal and is associated with augmented oxidative stress manifested by the depletion of serum antioxidant enzymes and increased excretion of oxidative modification products.
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PMID:Effects of oxidative stress on endothelial function after a high-fat meal. 1456 Dec 13

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h x day(-1), 5 days a week for 8 weeks, reaching the speed of 2.1 km x h(-1) at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km x h(-1) at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.
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PMID:Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat. 1468 69

To establish a monitoring system for gene expression profiles related to chemical contamination in wild common cormorants (Phalacrocorax carbo), the present study constructed an oligo array designed from expressed sequence tag (EST) sequences of the cormorant liver, where 1061 unique oligonucleotides were spotted. Common cormorants were collected from Lake Biwa, Japan in May 2001 and 2002. With the use of this oligo array, gene expression profiles in the liver of individual specimens were evaluated. To determine the expression patterns of genes altered by environmental contaminants, relationships between concentrations of persistent organochlorines including polychlorinated dibenzo-p-dioxins, furans, polychlorinated biphenyls, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane and its metabolites (DDTs), hexachlorocyclohexane isomers (HCHs), chlordane compounds (CHLs), butyltins, and bisphenol A (BPA) and expression levels of each gene in the cormorant liver were examined using stepwise multiple regression analysis. The reliability of data obtained by the oligo array was further confirmed by quantifying the expression levels of certain genes using real-time RT-PCR. The 2,3,7,8-tetrachlorodibenzo-p-dioxin toxic equivalent (TEQ) level was positively correlated with both cytochrome P4501A4 and 1A5 gene expression. In addition, the mRNA level of an antioxidant enzyme, Cu/Zn superoxide dismutase, was negatively correlated with hepatic total TEQ. Other antioxidant enzymes, glutathione peroxidase 3 and glutathione S-transferase class mu, were negatively correlated with HCHs and BPA levels, respectively. The mRNA expression level of a nonenzymatic antioxidant, haptoglobin, was negatively but not significantly correlated with CHLs. These results led to a hypothesis that wild cormorant population may suffer from oxidative stress due to chemically induced formation of reactive oxygen species and subsequent reduction of antioxidant resistance. Thus, the cormorant oligo array may be a useful monitoring tool to identify specific gene expression profiles altered by various environmental contaminants. Although further research is required to clarify a definitive cause-and-effect relationship, the current study provides valuable information on contaminant-responsive genes to predict potential effects on wildlife in a real environment.
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PMID:Gene expression profiling in common cormorant liver with an oligo array: assessing the potential toxic effects of environmental contaminants. 1650 60

Large mafs are transcriptional factors and members of the basic leucine zipper (b-Zip) superfamily. Since we previously identified expression of c-maf in mouse kidney, we presently investigated the mRNA expression profile in the kidney of c-maf gene knockout mice by using DNA microarray, and plasma glutathione peroxidase-3 (GPx3) was predominantly downregulated. We focused on the relation between the expression level of c-maf and GPx3 in vivo and in vitro. Since GPx3 is an antioxidant enzyme, oxidative stress was induced by exposing a culture cell derived from mouse renal tubules (mIMCD3) to hydrogen peroxide. Real-time PCR demonstrated that mRNA expression of both c-maf and GPx3 increased in parallel during exposure to oxidative stress in a time- and dose-dependent manner. Then, the mIMCD3 cells were transfected with c-maf-cDNA containing plasmid, which resulted in an increase in mRNA and protein expression of GPx3 compared with the control cells. Thus, c-maf may be transcriptional regulator of GPx3 expression and modulate the antioxidative pathway in the kidney.
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PMID:Correlation between the expression level of c-maf and glutathione peroxidase-3 in c-maf -/- mice kidney and c-maf overexpressed renal tubular cells. 1689 Jan 89

Maple syrup urine disease (MSUD) is an inherited disorder caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex activity. In the present study we evaluated selenium levels in plasma from MSUD patients at diagnosis and under treatment and the activities of glutathione peroxidase, catalase and superoxide dismutase in erythrocytes from treated patients. We verified that MSUD patients present a significant selenium deficiency at diagnosis, which becomes more pronounced during treatment, as well as a decrease of erythrocyte glutathione peroxidase activity during treatment. In contrast, erythrocyte catalase and superoxide dismutase activities were not altered in these patients. Our present results suggest that the reduction of an important antioxidant enzyme activity may be partially involved in the pathomechanisms of this disorder and that plasma selenium levels must be corrected through dietary supplementation in MSUD patients.
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PMID:Erythrocyte glutathione peroxidase activity and plasma selenium concentration are reduced in maple syrup urine disease patients during treatment. 1757 89

Glutathione peroxidase 3 (Gpx3) is ubiquitously expressed and is important antioxidant enzyme in yeast. It modulates the activities of redox-sensitive thiol proteins, particularly those involved in signal transduction pathway and protein translocation. Through immunoprecipitation/two-dimensional gel electrophoresis (IP-2DE), MALDI-TOF mass spectrometry, and a pull down assay, we found glutamine synthetase (GS; EC 6.3.1.2) as a candidate interacting protein with Gpx3. GS is a key enzyme in nitrogen metabolism and ammonium assimilation. It has been known that GS is non-enzymatically cleaved by ROS generated by MFO (thiol/ Fe(3+)/O(2) mixed-function oxidase) system. In this study, it is demonstrated that GS interacts with Gpx3 through its catalytic domain both in vivo and in vitro regardless of redox state. In addition, Gpx3 helps to protect GS from inactivation and degradation via oxidative stress in an activity-independent manner. Based on the results, it is suggested that Gpx3 protects GS from non-enzymatic proteolysis, thereby contributing to cell homeostasis when cell is exposed to oxidative stress.
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PMID:Glutathione peroxidase 3 of Saccharomyces cerevisiae suppresses non-enzymatic proteolysis of glutamine synthetase in an activity-independent manner. 1770 71

The purpose of this study was to determine the changes of both oxidant and antioxidant levels with exercise training in obese middle-aged women. The association between telomere length and oxidative stress with exercise was also examined. Sixteen obese middle-aged women participated in this study. The subjects were randomly divided into exercise group (EX) and control group (CON). EX performed aerobic exercise training for 6 months. DNA was extracted from leukocytes in peripheral blood and their telomere lengths were measured by real time PCR analysis. Long-term exercise training decreased body weight and BMI, and increased VO2 max. Resting levels of erythrocyte glutathione peroxidase activity were higher in EX compared to CON. Superoxide dismutase (SOD) activities were higher after the acute exercise test at mid-intensity in post-exercise training than in the pre-exercise training conditions. The telomere length did not change significantly after the acute exercise test in the pre-exercise training condition in spite of the increased level of malondialdehyde (MDA) as a marker of oxidative stress. In conclusion, antioxidant enzyme activities were increased following long-term exercise training; however, the lengths of telomere in leukocytes were not influenced by both mid-intensity and high intensity of exercise stress.
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PMID:Exercise training improves the antioxidant enzyme activity with no changes of telomere length. 1829 22

Our aim was to study the possible alterations of redox status (enzymatic and nonenzymatic parameters and metal elements) in erythrocytes of patients with hepatocellular carcinoma (HCC), colorectal liver metastases (CRLM) and benign liver neoplasms. The function of redox homeostasis is closely connected to the energy level of erythrocytes, therefore, the ATP level was also determined. Antioxidant parameters, enzyme activities of superoxide dismutase and glutathione peroxidase were estimated in the erythrocytes of 11 patients with benign tumour, 23 patients with primary malignant and 37 metastatic liver tumour patients and 30 age-matched and sex-matched healthy controls. Element content with inductively coupled plasma optical emission spectrometer and ATP level by the chemiluminometric method were also determined from the samples. Free radical intensity was significantly increased, whereas erythrocyte glutathione peroxidase and superoxide dismutase activities were significantly decreased in the HCC and CRLM groups versus benign groups and controls. Se, Mn and Zn levels were lowered in HCC and CRLM groups versus benign and control groups. The content of Cu, Mg, Se and Zn changed significantly between HCC and CRLM groups. Similarly, ATP concentration decreased in HCC and CRLM versus controls and benign groups. The lowest levels of ATP and antioxidant enzyme activities were found in the case of CRLM patients. These results reveal an alteration in the ATP level of erythrocytes with concomitant changes in the antioxidant defence system in hepatic cancer patients. Altered redox homeostasis (oxidative damage) may lead to decreased ATP level and consequently may play an important role in primary carcinogenesis and generation of metastases, as well.
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PMID:Oxidative stress with altered element content and decreased ATP level of erythrocytes in hepatocellular carcinoma and colorectal liver metastases. 1840 40

The aim of the present study is to evaluate the status of plasma essential trace elements magnesium (Mg), copper (Cu), zinc (Zn), iron (Fe) and selenium (Se) concentrations and their some related antioxidant enzyme activities, erythrocyte glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities in patients with Alzheimer's disease (AD). Fifty patients with AD and fifty healthy control subjects were included in this study. Plasma Cu and Zn concentrations by atomic absorption spectrometry (AAS), plasma Mg and Fe concentrations by spectrophotometric methods and plasma Se concentrations by graphite furnace AAS were determined. Erythrocyte GPx, SOD and CAT activities were measured by spectrophotometric methods. Plasma Mg, Cu, Zn, Fe and Se levels and erythrocyte GPx, SOD and CAT activities were found to be significantly lower in patients with AD compared with controls. These results suggest that alterations in essential trace elements and their related enzymes may play a role in the etiopathogenesis of AD. Also, there is a defect in the antioxidant defense system, which may lead to oxidative damage in patients with AD. The changes in antioxidant enzyme activities may be secondary to the alterations in their cofactor concentrations.
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PMID:Alterations of plasma magnesium, copper, zinc, iron and selenium concentrations and some related erythrocyte antioxidant enzyme activities in patients with Alzheimer's disease. 2056 29

The risk of oxidative stress-related metabolic diseases increases with menopause and physical inactivity. We hypothesized that an 8-week Tai Chi (TC) training program (2 sessions in class; 2 sessions at home; 1-1:15/session) would improve antioxidant capacity and reduce cardiovascular risks in both pre- (n = 8) and postmenopausal (n = 7) sedentary women. Selected measures of physical fitness and blood parameters were analyzed before and after the program. Besides the well-known effects of TC on balance, flexibility, and maximum leg extensor strength, TC (1) increased erythrocyte glutathione peroxidase activity-an aerobic training-responsive antioxidant enzyme-and plasma total antioxidant status and (2) decreased plasma total homocysteine, a cardiovascular risk marker. In addition to being a low-velocity, low-impact, and relatively safe, TC is a suitable physical activity design for pre- and postmenopausal women to increase antioxidant defenses. Investigating breathing effects during TC movements would be an interesting area for further research in diseases prevention.
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PMID:Effects of tai chi training on antioxidant capacity in pre- and postmenopausal women. 2158 29


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