Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present work reports the survival capacity of a strain of Brevibacterium linens isolated from a French camembert cheese and the ensuing changes in cell composition. Exponentially growing cells were harvested, washed and resuspended with shaking in pH 8.0 buffer at 21 degrees C in the absence of a carbon source. The viability of this strain, assessed with slide cultures, is much less than that of coryneform bacteria isolated from soil samples, even though no cell lysis was detected. Intracellular RNA was rapidly consumed during the first few days although magnesium levels remained high. The quantity of DNA initially increased by 17% within 24 h and then remained stable during the 30 days of the experiment. During the same period, absorbance of the medium at 260 nm reached 2 absorbance units. Reserve polysaccharides in this strain are less abundant than in Arthrobacter and were rapidly consumed. Proteolysis was regular and thus maintained a pool of free amino acids which was greater than 60% of the initial value. There was a parallel accumulation of ammonia in the medium. Catalase activity decreased regularly during the first 80 h whereas the quantity of Adenosine-5'-triphosphate (ATP) dropped by 47% in 10 h, stabilizing at less than 10% of its initial value. Cell respiration declined very rapidly and was very low after 24 h.
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PMID:Survival of Brevibacterium linens during nutrient starvation and intracellular changes. 399 87

1. Homogenates of guinea-pig polymorphonuclear leucocytes were separated by differential centrifugation into six particulate fractions and a soluble fraction. 2. The distributions in these fractions of protein, DNA, succinate dehydrogenase, beta-glucuronidase, peroxidase, alkaline phosphatase, acid phosphatase (against p-nitrophenyl phosphate and beta-glycerophosphate), cathepsin, and catalase were compared. 3. Almost all of the DNA sedimented in the first two pellets, indicating that the nuclei were relatively intact. 4. The four hydrolases and peroxidase showed different distribution patterns, although these activities were previously reported to be localized mainly in the single ;granule' fraction isolated from leucocytes. 5. The particles containing peroxidase, acid phosphatase and alkaline phosphatase all exhibited latency. Maximum activity for each enzyme was obtained at roughly similar concentrations of Triton X-100. 6. The acid phosphatase of these cells was distributed between two populations of particles that differed in both sedimentation characteristics and density. The acid phosphatase(s) of the two populations showed slightly different substrate specificities. This bimodal distribution was not an artifact of the procedure used to elicit the cells. 7. Catalase was recovered almost entirely in the soluble fraction and showed no latency in freshly prepared homogenates. No urate oxidase was detected. 8. We conclude that the ;granule' fraction of the polymorphonuclear leucocyte, as isolated by previous workers, contains at least three, probably more, populations of particles with different enzyme contents, and that these cells probably do not contain peroxisomes.
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PMID:The distributions of some granule-associated enzymes in guinea-pig polymorphonuclear leucocytes. 541 96

Current evidence suggests that bleomycin toxicity may be attributable to its DNA degradative activity possibly via generation of free radicals and O2 metabolites as mediators. Since lipopolysaccharide (LPS) has been known to provide protection against O2 toxicity, which is correlated with increased activity of O2 metabolite-detoxifying enzymes, the effect of this agent on bleomycin-induced pulmonary fibrosis was examined. Endotracheal bleomycin administration caused increased lung collagen synthesis. A single intraperitoneal injection of LPS (500 micrograms/kg) at day zero significantly decreased these increases. Total bleomycin-induced lung collagen increase was also significantly reduced. LPS alone had no significant effect on total lung catalase activity. Glutathiione peroxidase activity, however, was significantly decreased by 15.8% compared to untreated animals at 2 days after LPS treatment and remained unchanged at other time points. In addition, superoxide dismutase activity was significantly elevated by 30% above untreated animals only at 14 days after LPS administration and remained unchanged at other time points. Endotracheal bleomycin administration alone caused significant reductions in catalase activity at 2 days and 2 weeks after treatment, whereas glutathione peroxidase activity increased above control untreated animals at 2 and 4 weeks, respectively. Superoxide dismutase activity was unaffected by bleomycin treatment. Pretreatment with LPS before bleomycin prevented these reductions or caused increases in the activities of these enzymes at 2 days. Glutathione peroxidase was increased and was significantly greater than those animals treated with bleomycin alone. Catalase also was higher in the LPS plus bleomycin group (by 22.2%, p less than 0.05) than the bleomycin group alone. Compared to the effects on lung collagen synthesis and content, LPS treatment resulted in much less dramatic changes in total lung antioxidant enzyme activities. This discrepancy between the intensity of LPS effects on lung O2 metabolite-detoxifying enzymes and that on pulmonary fibrosis implies that the LPS-ameliorating effect on pulmonary fibrosis could not be totally explained by increased ability to detoxify O2 metabolites. Rather, the data would favor the possibility that LPS inhibits bleomycin-induced pulmonary fibrosis either by its known immunosuppressive effects or some other unknown mechanism. The former would be in agreement with previous data which suggest that an intact immune response is necessary for complete expression of the fibrogenic response to bleomycin.
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PMID:Inhibition of bleomycin-induced pulmonary fibrosis by lipopolysaccharide. 620 76

The catalase T structural gene of Saccharomyces cerevisiae was cloned by functional complementation of a mutation causing specific lack of the enzyme (cttl). Catalase T-deficient mutants were obtained by UV mutagenesis of an S. cerevisiae strain bearing the cas1 mutation, which causes insensitivity of catalase T to glucose repression. Since the second catalase protein of S. cerevisiae, catalase A, is completely repressed on 10% glucose, catalase T-deficient mutant colonies could be detected under such conditions. A cttl mutant was transformed with an S. cerevisiae gene library in plasmid YEp13. Among the catalase T-positive clones, four contained overlapping DNA fragments according to restriction analysis. Hybridization selection of yeast mRNA binding specifically to one of the cloned DNAs, translation of this mRNA in cell-free protein synthesis systems, and demonstration of catalase T protein formation by specific immunoadsorption showed that the catalase T structural gene had been cloned. By subcloning, the gene was located within a 3.5-kilobase S. cerevisiae DNA fragment. As in wild-type cells, catalase T synthesis in cttl mutant cells transformed with plasmids containing this fragment is sensitive to glucose repression. By DNA-RNA hybridization, catalase T transcripts were shown to be present in oxygen-adapting cells but absent from heme-deficient cells.
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PMID:Isolation of the catalase T structural gene of Saccharomyces cerevisiae by functional complementation. 635 26

We report the isolation and sequence of partial cDNA clones coding for human catalase. These clones were recovered from a human fibroblast cDNA library by screening with mixtures of oligonucleotide probes deduced from the amino acid sequence of human erythrocyte catalase. A comparison of their nucleotide sequence with the known protein sequence and mapping of homologous DNA sequences to the short arm of chromosome 11 in somatic cell hybrids confirmed that they coded for catalase. One of these clones contained a 462-base insertion interrupting the coding sequence with stop codons in all three reading frames. The 5' and 3' ends of the insertion correspond to the donor and acceptor consensus sequences of introns. Inspection of clones lacking the insertion confirm the location of the splice sites. We suggest this clone corresponds to the product of reverse transcription of an unspliced mRNA species. The catalase gene is the closest genetic marker mapped to Wilms tumor, one of the most prevalent of childhood cancers. Catalase cDNA probes will be useful to the examination of mitotic recombination in the etiology of this disease and may provide a useful starting point to the search for the putative Wilms tumor gene.
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PMID:Isolation of human fibroblast catalase cDNA clones. Sequence of clones derived from spliced and unspliced mRNA. 654 44

Neutrophils have been implicated in the pathogenesis of pulmonary injury in many clinical entities, but in vitro studies of neutrophil-mediated pneumocyte damage are limited. To study the role of neutrophils in mediating pulmonary injury, we cocultured these cells with monolayers of human A549 pneumocytes and rat type II alveolar cells. As indexes of injury, we measured cell detachment from monolayers, frank cytolysis, and the effect on pneumocyte protein and DNA synthesis. Unstimulated neutrophils effected minimal lysis or detachment of both pneumocyte targets, but neutrophils stimulated with phorbal myristate acetate and other secretogogues produced marked target cell detachment without lysis, which was time- and dose-dependent. Supernatants of activated neutrophils were similarly effective, suggesting that the mediator was a stable, soluble substance. Catalase and superoxide dismutase were minimally inhibitory to neutrophil-mediated detachment, and neutrophils from patients with chronic granulomatous disease produced detachment comparable to that produced by normal neutrophils. Furthermore, target cells were quite resistant to reagent H2O2 and non-neutrophil-derived toxic oxygen species, further suggesting that oxidative injury was not a major factor in causing detachment. Target cells were susceptible to detachment by the neutral proteases, elastase and collagenase, whereas neutrophil-mediated detachment was markedly inhibited by neutral protease and elastase inhibitors. Human and bovine serum were also inhibitory, but not albumin or pepstatin A, an acid protease inhibitor. Furthermore, we found that activated neutrophils inhibited protein and DNA synthesis of pneumocyte targets, providing additional evidence that neutrophils cause nonlytic injury to pneumocytes. These studies indicate that stimulated neutrophils cause nonlethal injury to pneumocytes, as measured by detachment from monolayers, and inhibition of vital intracellular synthetic functions. The mechanism of detachment is through the action of granule neutral proteases, rather than toxic oxygen metabolites, and is probably due to degradation of the extracellular matrix of the pneumocytes. In vivo, detachment could lead to desquamation of alveolar cells and increased permeability of the epithelial barrier of the lung. Similarly, inhibition of protein and DNA synthesis could have profound effects on the normal function and replication of alveolar epithelium.
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PMID:The injurious effect of neutrophils on pneumocytes in vitro. 673 53

Hydrogen peroxide (H2O2) induces SCEs in V-79 Chinese hamster cells. The incorporation of BrdUrd sensitizes the cells to the action of H2O2, but damage leading to the formation of SCEs can also be induced in DNA not substitued with BrdUrd. Catalase leads to a complete reduction of the SCE-producing as well as the toxic effect. The amino acid L-cysteine does not reduce the H2O2-induced SCE-frequencies. The results yield information about the relevance of SCE investigations in vitro for the determination of DNA-damaging substances and about the effects of antimutagenic SH-compounds.
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PMID:Characterization of sister chromatid exchange induction by hydrogen peroxide. 707 78

Ferritin from horse spleen was found to cause severe chromosome aberrations in cultured Chinese hamster ovary cells. Ferritin at 15 to 170 microgram/ml was clastogenic and at higher doses was cytotoxic. At comparable concentrations of protein or iron, neither apoferritin nor complexed iron was clastogenic. Sulfhydryl compounds glutathione and cysteine reduced the cytotoxic and clastogenic activities of ferritin. Physiological concentrations of glutathione may normally be sufficient to protect cells from damage. The reducing agent ascorbate had little protective effect. Chelating agents varied in their inhibitory activity: ethylenediaminetetraacetic acid (hexadentate) greater than nitrilotriacetic acid (tetradentate) greater than salicylate (bidentate). 2,2'-Bipyridyl enhance the chromosome-damaging action of ferritin while histidine did not markedly alter the frequencies of aberrations. Catalase and superoxide dismutase showed no inhibitory activity. The mechanism of DNA damage may involve reduction of Fe(III) in the ferritin core to Fe(II), followed by reoxidation of Fe(II) with possible formation of free radicals.
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PMID:Chromosome-damaging activity of ferritin and its relation to chelation and reduction of iron. 719 42

DNA cleavage induced by metallothionein (MT) containing copper was investigated by a DNA sequencing technique. Reconstituted Cd7-MT showed no ability to cause DNA cleavage. Commercially available rabbit MT I caused DNA cleavage, suggesting that DNA cleavage is due to the metal contained in commercial Mt. Cu2Cd5-MT and Cu12-MT were prepared by the treatment of commercial rabbit MT I with [Cu(CH3CN)4]CIO4. Cu12-MT frequently induced an alteration of thymine residues, especially in the 5'-GTC-3' sequence, and piperidine treatment led to chain cleavage at the thymine residues. The site specificity was similar to that obtained with Cu(I) plus H2O2. H2O2 enhanced DNA cleavage induced by Cu12-MT. Catalase and a Cu(I)-specific chelating agent, bathocuproine, inhibited DNA cleavage. These results suggest that Cu(I) and H2O2 have important roles in the production of active species causing DNA cleavage. Commercial MT and Cu2Cd5-MT induced DNA cleavage much less than Cu12-MT, but gave particularly specific DNA cleavage. Cu2Cd5-MT induced cleavage specifically at the central guanine residue of the 5'-GGT-3' sequence. A similar cleavage pattern was obtained with commercial MT. No effect of piperidine treatment suggests that the DNA cleavage might not be due to base damage and/or liberation. The DNA cleavage was inhibited efficiently by EDTA, but not by bathocuproine and catalase. Experiments with DNA ligands, albumin, and denatured DNA suggest that commercial MT and Cu2Cd5-MT induce nonoxidative cleavage of the deoxyribose phosphate backbone through its DNA recognition. These two types of cleavage mechanisms are discussed in relation to the possible role of Cu-MT in carcinogenesis.
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PMID:Oxidative and nonoxidative mechanisms of site-specific DNA cleavage induced by copper-containing metallothioneins. 761 16

Hyperplastic nodular cirrhosis was induced in rats by long-term (6 month) i.p. administration of thioacetamide at doses of 2.66 mmol/kg body wt, three times per week. The survival rate of animals at the end of the treatment was 90%. To follow the temporal changes samples at 0, 7, 15, 30, 45, 60, 90, 150 and 180 days from rats during thioacetamide intoxication and from chronological controls were obtained. The cirrhogenic ability of this treatment was assessed on the basis of morphological changes: the development of macronodular cirrhosis and the appearance of fibrous septa of collagen through portal spaces. Parameters of liver injury and cholestasis were obtained by assaying the serum activities of isocitrate dehydrogenase and gamma-glutamyltransferase. Enzymes and metabolites related to glutathione redox systems, as well as other antioxidant enzymes, were tested. Catalase and glutathione peroxidase, the two enzymes involved in the elimination of peroxides, and glutathione reductase decreased significantly at the end of the 6 months of intoxication, while Cu-Zn and Mn superoxide dismutases increased progressively during the long-term thioacetamide treatment. Protein thiol levels profile showed a biphasic change increasing from the 7th day and were insensitive to the 30% depletion of intracellular glutathione (GSH). To study the relationship of the intracellular thiols on the mechanisms of cell proliferation and differentiation during the cirrhogenic process, DNA content was assayed by flow cytometry in isolated hepatocytes, and DNA ploidy and distribution between G0-G1, S and G2 + M phases were determined. Remarkable changes in relation to a sharp increase in diploid population from 7 to 180 days (24.5%-->85.5%), a pronounced decrease in polyploid populations (tetraploid+octoploid) in the same period (73.7%-->12.3%), and elevations in the populations in S phase (S1 + S2) were observed in thioacetamide-treated rats. The results obtained indicate that hepatocytes isolated from thioacetamide-treated rats showed a marked tendency to diploidy, an enhancement in DNA replication parallel to the hepatic content of protein sulphydryl groups and a significant decline in antioxidant enzyme activities. The increase in protein thiols was independent of GSH level and of the thiol redox state.
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PMID:Relationship between antioxidant systems, intracellular thiols and DNA ploidy in liver of rats during experimental cirrhogenesis. 761 93


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