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)

E. coli thiol peroxidase (Tpx) linked to the thioredoxin as an in vivo thiol regenerating system acts as an antioxidant enzyme removing peroxides and H2O2. In order to elucidate the mechanism regulating tpx gene expression in E. coli in response to oxygen stress, we made 5' progressive deletions of upstream region from tpx gene, and fused to lacZ gene. LacZ activity was increased 6-fold by oxygen stress and inverted repeat sequence located between -47 and -33 nt was proven to be essential for the oxygen response of tpx promoter. Primer extension experiment and analysis of upstream sequence revealed transcription start point, -10, and -35 regions, which are in good agreements with the consensus sequences recognized by E sigma 70. Northern hybridization showed that expression of tpx gene is regulated at the transcriptional level. DNA binding assays using inverted repeat sequence including -35 region provides preliminary evidence that expression of tpx requires additional transcriptional factor in response to oxygen stress.
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PMID:Identification of promoter in the 5'-flanking region of the E. coli thioredoxin-linked thiol peroxidase gene: evidence for the existence of oxygen-related transcriptional regulatory protein. 863 14

Indian Childhood Cirrhosis (ICC) is a disease of abnormal copper metabolism commonly characterized by swelling and degeneration of liver cells along with the presence of orcein staining deposits of copper. Hepatic copper content of ICC patients was about 43 fold higher than those of control subjects. The data on sub-cellular distribution of copper revealed massive accumulation of Copper (73%) of total cell copper) in the nuclear fraction (455 micrograms Cu/g tissue nuclei). On further distribution of copper in nuclear fraction, the enrichment of copper in heterochromatin and euchromatin of ICC nuclei was found to be 48 and 15 fold higher over control fractions respectively. The ultra-violet spectra of heterochromatin and euchromatin isolated from ICC nuclear fraction showed a broad absorption maxima as compared to controls. Further, A260/A280 ratio was markedly lower in heterochromatin and euchromatin of ICC liver in comparison to controls. An antioxidant enzyme, catalase activity was also significantly reduced in ICC liver as compared to control. Further, DNA fragmentation studies indicated that there was significantly increased DNA fragmentation in ICC liver. Collectively, these findings suggest that massive accumulation of copper in nucleus and decrease in catalase activity was associated with DNA fragmentation in hepatocyte of ICC disease.
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PMID:Molecular basis of pathophysiology of Indian childhood cirrhosis: role of nuclear copper accumulation in liver. 870 72

Glutathione peroxidase is an antioxidant enzyme found in a diverse array of eukaryotic species. We have determined the DNA sequence of a glutathione peroxidase homolog in the pathogenic bacterium Neisseria meningitidis. The sequence displays features of a functional gene, but lacks a selenocysteine-encoding in-frame TGA codon characteristic of most mammalian glutathione peroxidase genes. The derived amino acid sequence encoded by the N. meningitidis homolog predicts a 19.9 kDa protein that displays a high level of amino acid identity with other gluathione peroxidase sequences, particularly within four conserved regions of the enzyme.
DNA Seq 1995
PMID:Identification of a glutathione peroxidase homolog in Neisseria meningitidis. 874 63

Reactive oxygen species (ROS) have been shown to impair sperm function. The actions of ROS are reduced by antioxidant enzymes, including catalase. Although catalase-like activity has been demonstrated in semen, there has been no localization or characterization of catalase mRNA expression in the male reproductive tract. Catalase mRNA levels were evaluated by northern blot analysis and in situ hybridization from the male reproductive organs of normal 60-day-old rats, testes of 10- to 90-day-old rats, and testes of rats subjected to efferent duct ligation. Radioactive DNA probes were synthesized using a Klenow polymerase-based specific primer synthetic procedure with a known published sequence for rat catalase. All tissues demonstrated a single transcript of 2.5 kilobases (kb). Low levels of catalase mRNA were detected in the normal testis, epididymis, vas deferens, and prostate. No expression was detectable with northern analysis in seminal vesicle. The levels of catalase mRNA in reproductive organs were compared with the high levels of expression detectable in rat liver. In the testis, catalase expression was primarily localized to peritubular and interstitial cells. In the epididymis and prostate, mRNA was detected in the epithelium. The observed decrease in catalase mRNA levels in the maturing rat testis is consistent with its interstitial localization. The increase in testicular catalase mRNA levels seen in parallel with progressive thinning of the germinal epithelium after efferent duct ligation is also in keeping with a peritubular or interstitial cell localization. The relatively low levels of catalase mRNA expression in the normal adult male reproductive tract undermine the role of catalase as a major antioxidant enzyme in these tissues. The low levels of catalase mRNA in the testis, and the undetectable levels in the seminiferous epithelium, however, imply that the germinal epithelium is predisposed to an oxidative state. These findings may help to explain the known susceptibility of the testis to oxidative stress.
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PMID:Catalase mRNA expression in the male rat reproductive tract. 895 90

Tolerance to hyperoxia usually depends on an increase in lung antioxidant enzyme activity. Antioxidant-surfactant liposomes, encapsulating the antioxidant enzymes CuZn-superoxide dismutase (CuZnSOD) and catalase in synthetic surfactant lipids, increase lung antioxidant activity following intratracheal instillation in premature and term rabbits. We investigated whether the exogenous antioxidant enzymes encapsulated in these liposomes inhibit the endogenous antioxidant enzyme synthesis in the premature rabbit lung. Premature rabbits, delivered at 28 days of gestation, were treated intratracheally with antioxidant-surfactant liposomes, surfactant liposomes without antioxidant enzymes, or air placebo at birth and exposed to hyperoxia for 24 h. A comparison group was killed after breathing room air at birth. The right lungs of the pups were assayed for CuZnSOD and catalase activities and DNA content, the left lungs of the same pups were used to quantitate the concentrations of CuZnSOD and catalase mRNA using cRNA probes. Lung CuZnSOD and catalase mRNA quantities increased during exposure to hyperoxia, but were not affected by exogenous antioxidant enzymes. These data suggest that intratracheal instillation of CuZnSOD and catalase does not down-regulate mRNA transcription of these antioxidant enzymes in the premature rabbit lung.
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PMID:Lung CuZn-superoxide dismutase and catalase gene expression in premature rabbits treated intratracheally with antioxidant-surfactant liposomes. 898 40

Oxidative damage is a proposed mechanism of asbestos-induced carcinogenesis, but the detection of oxidative DNA lesions in target cells of asbestos-induced mesothelioma has not been examined. In studies here, DNA was isolated from both rat pleural mesothelial (RPM) cells and a human mesothelial cell line (MET5A) after exposure in vitro to crocidolite asbestos at various concentrations. DNA was then examined for formation of 8-hydroxydeoxyguanosine (8-OHdG) at 24, 48 and 72 h using HPLC with electrochemical detection. In addition, steady-state mRNA levels of manganese-containing superoxide dismutase (MnSOD) were assessed as an indication of oxidative stress. Whereas RPM cells showed dose-dependent and significant increases in 8-OHdG formation in response to crocidolite asbestos or iron-chelated crocidolite fibers (but not after exposure to glass beads), MET5A cells showed decreases in 8-OHdG. Both cell types exhibited elevations in message levels of MnSOD. In comparison with human MET5A cells, RPM cells exhibited increased cytotoxicity and apoptosis in response to asbestos, as documented by cell viability assays and flow cytometry analysis using propidium iodide. Results in RPM cells indicate that asbestos causes oxidative damage that may result in potentially mutagenic lesions in DNA and/or apoptosis, despite compensatory increases in expression of an antioxidant enzyme.
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PMID:Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos. 911 Dec 21

Thioredoxin reductase from Escherichia coli is a dimeric enzyme containing one FAD and one redox-active disulfide per monomer and catalyzes the transfer of electrons from NADPH to thioredoxin, which subsequently performs several important cellular functions. To overcome problems with site-directed mutagenesis and low expression, the thioredoxin reductase gene was adapted for use in the plasmid vector pSL350 (Brosius, J., Methods Enzymol. 216, 469-483, 1992), which is designed both for protein expression and for production of single-stranded template DNA for mutagenesis, and examined expression of wild-type thioredoxin reductase under different growth conditions. In the absence of IPTG inducer, expression of thioredoxin reductase in saturated cultures accounts for 19% of the soluble protein, and with 1 mM IPTG expression increases to 61%. Some of the thioredoxin reductase is expressed as apoenzyme with the amount of apoenzyme increasing at higher IPTG concentrations, accounting for as high as 68% of the total thioredoxin reductase expressed. The apoenzyme in cell extracts is activated rapidly by addition of FAD, indicating correct folding of the enzyme in the absence of cofactor. Purification of wild-type thioredoxin reductase from the new system yielded 189 mg of enzyme from a 300-ml uninduced culture. The new plasmid was also used to generate an N155Y mutant which is purified and partially characterized.
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PMID:Application of a single-plasmid vector for mutagenesis and high-level expression of thioredoxin reductase and its use to examine flavin cofactor incorporation. 912 9

The effect of cadmium ion (Cd) and ascorbic acid (Asc) on the induction of oxidative DNA damage and on the activities of antioxidant enzymes were investigated in human lymphoblastoid cells (AHH-1 TK+/-). Cd at low concentrations of 5-35 microM induced the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and caused nuclear DNA strand breaks. The formation both of 8-OHdG and of DNA strand breaks was dose-dependent at the low Cd concentration; both parameters were linearly correlated with each other (R = 0.932 and P = 0.0209). 8-OHdG formation by Cd plateaued at a Cd concentration of 50 microM. Asc also induced 8-OHdG formation, but it had no synergistic effect with Cd on the formation of 8-OHdG or DNA strand breaks. Cd at the concentration of 50 microM induced the nuclear activity of the antioxidant enzymes, catalase and superoxide dismutase (SOD). Furthermore, Cd caused a decrease in the concentration of reduced glutathione (GSH) and an increase in concentration of the oxidized form (GSSG). While Asc had no observable effect on SOD activity, it did increase nuclear catalase activity in cells. This effect on catalase was synergistic with that of Cd. The linear correlation between 8-OHdG and DNA strand breaks induced by Cd at the lower Cd concentrations (< or = 50 microM), suggested that the extent of formation of DNA strand breaks induced by Cd may be offset by their induction of the formation of 8-OHdG and antioxidant enzyme activities.
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PMID:Cadmium-induced 8-hydroxydeoxyguanosine formation, DNA strand breaks and antioxidant enzyme activities in lymphoblastoid cells. 914 17

The effects of the flavonoids quercetin, myricetin and silymarin on DNA damage and cytotoxicity in human cells were investigated. DNA strand breaks and oxidised pyrimidines were determined using alkaline single cell gel electrophoresis (the comet assay). Inhibition of cell growth was also measured. Caco-2 (colon), HepG2 (liver), HeLa (epithelial) cells and normal human lymphocytes showed different, dose-dependent susceptibilities (in terms of strand breakage) to the various flavonoids, quercetin being the most damaging. This agreed well with the ability of the flavonoids to inhibit cell growth. None of the flavonoids induced DNA base oxidation above background levels. All of the flavonoids under investigation caused depletion of reduced glutathione, which, in the case of quercetin, occurred prior to cell death. Neither cytotoxicity nor genotoxicity was associated with the antioxidant enzyme capacity (glutathione, glutathione reductase, glutathione peroxidase and catalase) of the cells.
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PMID:The effect of dietary flavonoids on DNA damage (strand breaks and oxidised pyrimdines) and growth in human cells. 915 Jul 62

An oxidant stress has been shown to prevail in experimental and clinical nephrotic syndrome. Such oxidant stress may be induced by a reduced activity of antioxidant systems. We examined the altered expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, in patients with idiopathic nephrotic syndrome, in whom an increased oxidant stress had been demonstrated. The Mn-SOD activities in peripheral blood mononuclear cells obtained from 12 patients with active nephrotic syndrome (6.0 +/- 1.1 years of age, mean +/- SE) and hypoproteinemia were 42% lower (p < 0.05) than in 12 control subjects (5.5 +/- 0.5 years of age) with normal serum total protein concentrations. Reverse-transcriptase polymerase chain reaction also demonstrated that Mn-SOD messenger RNA expression in the patients with nephrotic syndrome was, on average, 59% lower than in control subjects. Because expressions of some genes are sensitive to serum, the serum dependency of Mn-SOD gene transcription was studied in glomerular endothelial cells transfected with a luciferase reporter gene fused with a rat Mn-SOD DNA fragment of -806 to +22 bp of the transcription initiation site (-806:+22). When these cells were exposed to different concentrations of fetal bovine serum (0.5% to 15%), the transcriptional activities determined by luciferase activities were proportional to serum concentrations. This serum-dependent transcriptional activation was also demonstrated by the fragment (-220:+22) but not by the fragment (-220:-20). When glomerular endothelial cells transfected with the fragment (-220:+22) were treated with 5% serum from patients with active nephrotic syndrome, transcriptional activation was more than 80% less than that by 5% serum from control subjects without nephrosis. These results indicate that Mn-SOD gene transcription is regulated at least in part by serum, and that the serum-dependent transcription of the gene is diminished in patients with idiopathic nephrotic syndrome. The regulatory region of serum-dependent gene transcription resides within its early promoter region. Our findings suggest that down-regulation of antioxidant enzyme transcription may contribute increased oxidant stress in idiopathic nephrotic syndrome.
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PMID:Down-regulation of manganese-superoxide dismutase gene expression in idiopathic nephrotic syndrome. 915 91


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