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)

Parenteral iron has been recommended for the treatment of iron deficiency in the majority of maintenance hemodialyzed (HD) patients. However, iron supplementation and consequent over saturation of transferrin and high iron levels, may aggravate oxidative stress already present in these patients. This study aimed to further clarify the role of repeated intravenous iron therapy as a supplementary cause of oxidative stress in HD patients. Markers of free radical activities (carbonyl reactive derivatives, CRD, thiol groups, SH, malondialdehyde, MDA) and antioxidant enzyme activities (superoxide dismutase, SOD and glutathione peroxidase, GPX) were determined in plasma and red blood cells (RBC) of 19 hemodialysis patients given a total iron dose of 625 mg (ferrogluconat, Ferrlecit, 62.5 mg). Blood samples were taken before the first and after the last dose of iron. Twenty apparently normal subjects served as healthy controls. Before iron treatment, HD patients exhibited increased concentrations of MDA and CRD in plasma and red blood cells, accompanied with impaired antioxidant capacity. All patients responded to iron therapy with a significant increase in their serum ferritin, serum iron, hemoglobin, and red blood cells levels. However, iron treatment resulted in enhanced oxidative stress in plasma of HD patients, since significant increase in plasma MDA and CRD concentrations, together with a decrease in nonprotein SH groups levels were detected. Supplementation with iron did not significantly influence plasma SOD and GPX activities, nor did any of the red blood cell parameters tested. Our data show that, despite improvement in hematological parameters, an increase in iron stores due to supplementation could also contribute to increased free radical production in HD patients.
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PMID:Evaluation of oxidative stress after repeated intravenous iron supplementation. 1595 53

Catalase is a highly conserved heme-containing antioxidant enzyme known for its ability to degrade hydrogen peroxide into water and oxygen. In low concentrations of hydrogen peroxide, the enzyme also exhibits peroxidase activity. We report that mammalian catalase also possesses oxidase activity. This activity, which is detected in purified catalases, cell lysates, and intact cells, requires oxygen and utilizes electron donor substrates in the absence of hydrogen peroxide or any added cofactors. Using purified bovine catalase and 10-acetyl-3,7-dihydroxyphenoxazine as the substrate, the oxidase activity was found to be temperature-dependent and displays a pH optimum of 7-9. The Km for the substrate is 2.4 x 10(-4) m, and Vmax is 4.7 x 10(-5) m/s. Endogenous substrates, including the tryptophan precursor indole, the neurotransmitter precursor beta-phenylethylamine, and a variety of peroxidase and laccase substrates, as well as carcinogenic benzidines, were found to be oxidized by catalase or to inhibit this activity. Several dietary plant micronutrients that inhibit carcinogenesis, including indole-3-carbinol, indole-3-carboxaldehyde, ferulic acid, vanillic acid, and epigallocatechin-3-gallate, were effective inhibitors of the activity of catalase oxidase. Difference spectroscopy revealed that catalase oxidase/substrate interactions involve the heme-iron; the resulting spectra show time-dependent decreases in the ferric heme of the enzyme with corresponding increases in the formation of an oxyferryl intermediate, potentially reflecting a compound II-like intermediate. These data suggest a mechanism of oxidase activity involving the formation of an oxygen-bound, substrate-facilitated reductive intermediate. Our results describe a novel function for catalase potentially important in metabolism of endogenous substrates and in the action of carcinogens and chemopreventative agents.
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PMID:Characterization of the oxidase activity in mammalian catalase. 1607 30

In the apical meristem of Allium fistulosum, the relationship between peroxide lipid oxidation, antioxidant activity, proliferative processes, the yield of chromosomal aberrations and duration the exposure to ionized air was studied. Under the influence of air oxygen ions, superoxide dismutase and catalase activities increased, proliferative processes were stimulated, and shifts occurred in the process of lipid peroxidation in cells of A. fistulosum. When these cells were treated with air oxygen for 40 min, hydrogen peroxide and iron sulfate (II) enhanced oxygen biostimulating effect via stimulation of antioxidant enzyme activity and inhibition of lipid peroxidation. Under these conditions, cell proliferation was intensified and the yield of chromosomal aberrations was reduced in A. fistulosum rootlets. When the time of seed treatment with ionized air was increased to 80 min, lipid peroxidation was activated, antioxidant enzyme activity was inhibited, and the yield of chromosomal aberration increased in seedlings. It was concluded that the biostimulating activity of ionized air was mediated by active oxygen species generated in the cell. The accumulation of TBA(thiobarbituric acid)-reactive products was shown to be related to a decrease in antioxidant enzyme activity and an increase in the yield of chromosomal aberrations. It is emphasized that the mutagenic effect of ionized air is associated with generating conditions that support Fenton reaction and OH-radical formation in the cell.
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PMID:[Mitogenic and mutagenic effects of ionized air on Allium fistulosum L]. 1624 Jun 34

Fatty acid has been reported to be associated with cardiovascular diseases and cancer, but the possible mechanism remains unclear. Here, we reported a novel mechanism for the permissive role of fatty acid on iron intracellular translocation and subsequent oxidative injury. In vitro study from endothelial cells showed that iron alone had little effect, whereas in combination with PA (palmitic acid), iron-mediated toxicity was markedly potentiated, as reflected in mitochondrial dysfunction, cell death, apoptosis, and DNA mutation. We also showed that PA not only facilitated iron translocation into cells through a transferrin-receptor (TfR)-independent mechanism, but also translocated iron into mitochondria; the subsequent intracellular iron overload resulted in reactive oxygen species (ROS) overgeneration and lipid oxidation. Further investigation revealed that PA-facilitated iron translocation is due to Fe/PA-mediated extracellular oxidative stress and the subsequent membrane damage with increased membrane permeability. Fe/PA-mediated toxic effects were reduced in rho0 cells lacking mitochondrial DNA or by antioxidant enzyme SOD, especially mitochondrially localized MnSOD, suggesting a permissive role of PA for iron deposition on the vascular wall and its subsequent toxicity via mitochondrial oxidative stress. This observation was confirmed in vivo in mice, wherein higher vascular iron deposition and accompanying superoxide release were observed in the presence of a high-fat diet with iron administration.
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PMID:Fatty acid-mediated intracellular iron translocation: a synergistic mechanism of oxidative injury. 1625 39

Different kinds of oxidative stress cause responses of antioxidant defenses which often act in concert. In previous works, some relationships have been found between oxidative stress markers and antioxidant enzyme activities in goldfish treated with different levels of oxygen or heat shock. This study aimed to check whether or not there are general patterns of relationships between antioxidant enzyme activities and oxidative stress indices in goldfish tissues, regardless of the stressor. For this, goldfish were treated with different concentrations of iron sulphate, 20 or 500 microM, as well as limestone water for 7 days. Both iron ions and limestone water led to a pH shift. Therefore, complex effects of iron ions and/or a pH shift on levels of oxidative stress indices and antioxidant enzyme activities in goldfish liver and kidney were investigated. Experimental conditions resulted in increased protein carbonyl content by 1.5-1.9-fold. Externally added iron ions did not change lipid peroxide levels in the liver but decreased them in the kidney, while levels of thiobarbituric acid reactive substances (TBARS) were elevated by 1.4-2.5-fold. Limestone water raised levels of both lipid peroxidation products in the liver. The treatment affected activities of superoxide dismutase and catalase only slightly, but activities of glutathione-associated enzymes, glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH) were lowered in many cases. G6PDH activities correlated inversely with protein carbonyl levels (R2 = 0.77-0.97), suggesting possible inactivation of the enzymes due to their carbonylation. Levels of lipid peroxidation products had a positive correlation to activities of catalase in the liver and GR in the kidney (R2 = 0.83), indicating possible up-regulation of the enzymes by these products. A negative link between TBARS levels and GST activities may reflect the involvement of GST in the detoxification of lipid peroxide products. The main conclusions are: (i) experimental conditions resulted in increased levels of protein carbonyls and end products of lipid peroxidation (TBARS); (ii) under oxidative stress, some enzymes can be inactivated due to oxidation; (iii) lipid peroxidation products seem to be involved in up-regulation of some antioxidant enzymes.
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PMID:Coordinated response of goldfish antioxidant defenses to environmental stress. 1673 67

1. The aim of the study was to evaluate the effects of alpha-tocopheryl acetate (50 mg/kg) and beta-carotene (15 mg/kg) dietary supplementation on the oxidative status of raw turkey breast and leg muscles assessed by thiobarbituric acid test values, the vitamin E levels and the antioxidant enzyme activities. In parallel, a quantitative descriptive sensory analysis was carried out on cooked, stored and reheated samples. 2. Vitamin E was present in sufficient quantity to reduce oxidation, since iron-induced reactive substances (TBARS) were significantly lower in antioxidant-supplemented treatments. The results suggested that the presence of beta-carotene in the diet limits the accumulation of alpha-tocopherol in turkey muscles. 3. In the present study, there was no conclusive relationship between dietary antioxidant supplementation and endogenous antioxidant enzyme activities. 4. Sensory evaluation showed that a longer supplementation time and dose may be necessary in turkeys to prevent meat from rancidity and warmed-over flavour (WOF). Leg pastiness and stringiness were modified by dietary antioxidant supplementation, indicating the possible synergism between antioxidants and cysteine proteinases in the perception of meat quality. 5. Given the modern trends that lead consumers to increase their consumption of poultry meat, it would be interesting to evaluate the commercial potential and cost effectiveness of routine dietary antioxidant supplementation.
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PMID:Effects of alpha-tocopheryl acetate and beta-carotene dietary supplementation on the antioxidant enzymes, TBARS and sensory attributes of turkey meat. 1719 Jun 77

An exposure of isolated rat brain genomic DNA to oxidative stress in the form of iron salts (Fe2+) and ascorbate results in gene-specific DNA lesions detectable by a quantitative polymerase chain reaction (PCR) based assay in which PCR amplification efficiency of the affected genes (e.g. beta-actin and p53) is grossly impaired. Such oxidative DNA lesions are prevented by hydroxyl radical scavengers like mannitol (20 mM) and sodium benzoate (20 mM) or by the antioxidant enzyme catalase (50 microg/ml) present in the incubation mixture during exposure to Fe2+ and ascorbate. When brain DNA isolated from young (4-6 months of age) and aged (20-24 months of age) rats are analyzed similarly by the PCR based method, the amplification levels of beta-actin and p53 genes are noticeably decreased in the case of aged rat indicating an accumulation of gene-specific DNA lesions during brain aging.
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PMID:Gene-specific oxidative lesions in aged rat brain detected by polymerase chain reaction inhibition assay. 1736 57

We have studied the effect of resveratrol on lipoperoxidation and antioxidant enzyme activity level in the brain of healthy rats. When intraperitoneally administered, resveratrol significantly and dose dependently decreased brain malondialdehyde level. Resveratrol also increased in a dose-dependent way brain superoxide dismutase, catalase and peroxidase activities. Optimal effect on antioxidant enzyme and lipoperoxidation products were obtained with resveratrol concentration of 12.5 mg/kg body wt. Native polyacrylamide gel electrophoresis analysis of antioxidant isoenzymes revealed that resveratrol up regulated at least two acidic superoxide dismutase isoforms called A(1) and A(2), two basic isoforms called B(1) and B(2). Resveratrol also up regulated two catalase isoforms and a broad peroxidase band corresponding to several isoforms. All these findings suggest that resveratrol is able to cross the blood brain barrier and exerts potent antioxidant features. Resveratrol also exerts neuroprotective properties by up regulating several detoxifying enzymes, most of which are iron proteins.
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PMID:Effect of resveratrol on antioxidant enzyme activities in the brain of healthy rat. 1740 79

Phellinus linteus (PL) mushroom has been reported to possess antioxidant activity. The present study was designed to investigate whether an ethanol extract obtained from PL might ameliorate oxidative stress and enhance antioxidant enzyme activities in primary rat hepatocytes, which were overloaded with iron using ferric nitrilotriacetate (FeNTA) complex. FeNTA enables hepatocytes to accumulate substantially redox-active iron and stimulates the production of injurious hydroxyl radicals, which in turn, initiate oxidative stress-mediated cytotoxicity. The results showed that pretreatment of hepatocytes with PL extract (50, 100 and 200 microg/mL) for 24 h significantly reversed FeNTA-induced cell viability loss, lactate dehydrogenase leakage (LDH), lipid peroxidation (LPO) and protein carbonyl formation in a dose-dependent manner. It was further observed that PL extract produced an inhibitory effect on intracellular reactive oxygen species (ROS) formation caused by FeNTA. Concomitantly, the amount of GSH content and the activities of glutathione reductase (GSH Rd) and glutathione peroxidase (GSH Px) in hepatocytes pretreated with PL extract increased substantially compared with those treated with FeNTA alone. These results suggest that PL may be useful in protecting against FeNTA-induced oxidative damage and also be capable of attenuating cytotoxicity of other oxidants.
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PMID:Protective effects of Phellinus linteus extract against iron overload-mediated oxidative stress in cultured rat hepatocytes. 1760 36

The aim of this work is to study the level of oxidative stress in blood of beta-thalassemia major patients with transfusional iron overload and chelation therapy as a central pathological process. Beta-thalassemia major results in an increase in the concentration of lipid peroxidation products in blood plasma of more than 100% and in the intensity of chemiluminescence - about 20% in comparison to healthy controls. The activity of the antioxidant enzyme superoxide dismutase in the blood of beta-thalassemia major patients is decreased by more than 30% and the total antioxidant activity is diminished by about 70% compared to controls. Experimental data confirm the progression of oxidative stress in patients with beta-thalassemia major: activation of free radical processes and lipid peroxidation, decreased antioxidant capacity. Strong oxidative damage and essential alternations define these parameters as sensitive markers of oxidative stress in patients with beta-thalassemia major. The combination of effective iron-chelatory agents with natural or synthetic antioxidants can be extremely helpful in clinical practice in the regulation of the antioxidant status of patients with beta-thalassemia major.
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PMID:Oxidative stress in patients with beta-thalassemia major. 1792 25


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