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)

Hydrogen peroxide-resistant Chinese hamster ovary (CHOR) cells were developed by exposing parental (CHO(P)) cells to sequential increases in H2O2 concentration. Cytotoxicity as well as DNA single-strand breaks induced by Na2CrO4 were then compared in CHOR and CHO(P) cell lines. Using the colony-forming assay, it was found that the cytotoxicity caused by Na2CrO4 did not differ in the parent and resistant cells. However, alkaline elution studies showed that the production of DNA single-strand breaks in CHOR cells treated with Na2CrO4 was reduced by about 50% as compared with that in CHO(P) cells. Similarly, electron spin resonance (ESR) studies revealed that the level of chromium(V) in CHOR cells during treatment with Na2CrO4 was about 50% that in CHO(P) cells. CHOR cells were also found to be cross-resistant to the cytotoxicity and DNA breaks caused by other toxic metals such as CdCl2 and HgCl2. Catalase activity in resistant cells was 2-fold and the cellular content of glutathione was 3-fold that in parental cells. However, no obvious differences were seen in superoxide dismutase and glutathione reductase activity, although the contents of ascorbic acid or alpha-tocopherol were slightly decreased in CHOR cells, suggesting that the resistance in CHOR cells may be associated with the increase in both catalase activity and glutathione contents in cells. These results indicate that chromate-induced DNA breaks appear to be mediated by a different mechanism than that for the cytotoxicity of this metal, and also suggest that the formation of active oxygen species and/or chromium(V) during reduction of chromium(VI) inside cells might be associated with the induction of the DNA strand breaks caused by the metal.
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PMID:DNA single-strand breaks and cytotoxicity induced by sodium chromate(VI) in hydrogen peroxide-resistant cell lines. 768 Apr 28

The addition of catalase isolated from bovine liver to the culture medium of quiescent mouse osteoblastic MC3T3-E1 cells decreased intracellular oxidized state, determined using fluorescent dye and laser-scanning confocal microscopy. The decrease in intracellular oxidized state evoked by catalase seemed to be involved in the arrest of growth, since catalase increased the incorporation of [3H]thymidine in these quiescent cells. On gel filtration of the catalase preparation, catalase activity and the stimulation of DNA synthesis coincided. Of the early response genes, JE, which is induced by competence factors, was induced by catalase in this cell line, whereas c-fos, c-jun, and KC mRNA levels were not affected. Catalase isolated from fungi and glutathione peroxidase+glutathione added to the culture medium also increased the steady-state level of JE mRNA. These results indicate that cells in the quiescent state produce hydrogen peroxide endogenously and that hydrogen peroxide acts as one of the mediators inhibiting DNA synthesis as well as the expression of JE, a growth factor-inducible gene.
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PMID:Activation of DNA synthesis and expression of the JE gene by catalase in mouse osteoblastic cells: possible involvement of hydrogen peroxide in negative growth regulation. 773 53

The incubation of lambda DNA in the reaction system of alloxan plus NADPH-cytochrome P450 reductase (fp2) in the presence of ferritin caused strand breaks after a lag time of about 5 min. Addition of ferritin to the reaction system at concentrations below 50 micrograms/ml caused the strand breaks of DNA in a concentration-dependent fashion. Catalase, scavengers of hydroxyl radicals (HO.) and iron-chelators almost completely inhibited the DNA strand breaks, but superoxide dismutase (SOD) did not, suggesting that the strand breaks are induced by the generation of HO. via the reaction of H2O2 and Fe(II), namely, the Fenton reaction. When the ferritin was incubated in the reaction system of alloxan plus fp2, the iron release from ferritin increased with incubation time depending on the amount of fp2. The addition of increasing concentrations of ferritin to the reaction system resulted in progressive increase in the iron release and a decrease in the electron spin resonance signal intensity of alloxan radical (HA.), the one electron reduced form of alloxan, suggesting that HA. generated in the reaction system is capable of releasing iron from ferritin. These results support the possibility that the iron released from ferritin may be involved in the diabetogenic action of alloxan.
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PMID:Effect of ferritin on lambda DNA strand breaks in the reaction system of alloxan plus NADPH-cytochrome P450 reductase: ferritin's role in diabetogenic action of alloxan. 774 95

To study the relative sensitivity of rat tracheal epithelial and mesothelial cell DNA to oxidant damage, we used the comet assay, a gel microelectrophoresis method that allows visual determination of DNA strand breaks on a cell-by-cell basis, to evaluate damage after hydrogen peroxide exposure. By both a qualitative and a quantitative assay, tracheal epithelial mesothelial cells demonstrated a similar dose-response increase in the number of cells showing strand breaks and the number of breaks per cell after exposure to increasing concentrations of hydrogen peroxide; but even at the highest concentration, some cells failed to show damage. By contrast, 100% of cultured V79 lung fibroblasts showed evidence of damage. Catalase and deferoxamine largely prevented the formation of strand breaks, while superoxide dismutase was not protective. To evaluate DNA repair, cells were exposed to 10 microM hydrogen peroxide for 10 min, washed, and maintained in culture medium; by 2 h the proportion of mesothelial and epithelial cells showing comets had returned to control levels for both cell types. Both cell types also showed a similar pattern of increasing damage after continuous exposure to 10 microM hydrogen peroxide for periods up to 2 h. We conclude that, in this system, 1) mesothelial and tracheobronchial epithelial cells show a similar pattern of DNA injury and repair after hydrogen peroxide exposure; 2) hydrogen peroxide damages DNA of both cell types via a mechanism probably related to the iron-catalyzed formation of hydroxyl radical; and 3) both types of cells appear to be heterogeneous in their sensitivity to oxidant damage, with some cells showing extreme resistance to such damage.
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PMID:Rat mesothelial and tracheal epithelial cells show equal DNA sensitivity to hydrogen peroxide-induced oxidant injury. 776 85

The degree of DNA damage by the treatment with various molecular species of active oxygen and its inhibition by pretreatment with different scavengers were evaluated using pUC19 plasmid DNA. DNA damage caused by O2-. generated by xanthine-xanthine oxidase system (X-XOD), .OH by Fenton reactions, and OCl- by NaOCl involved the generation of open circle DNA demonstrating single strand breaks. Catalase (Cat), diethylenetriaminepentaacetic acid (DETAPAC), desferroxiamine (Desferal), dimethyl sulfoxide (DMSO) and ethanol (EtOH) all inhibited 60-80% of DNA damage by the generated O2-.. Superoxide dismutase (SOD) inhibited all DNA damages by O2-.. Cat, DETAPAC and Desferal effectively inhibited DNA break by .OH; complete inhibition of .OH-induced DNA break was achieved by addition of DMSO and EtOH. Desferal and EtOH completely inhibited DNA damage by OCl-. These findings suggested that metal ions are associated with the mechanism of DNA damage by all forms of active oxygen species.
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PMID:DNA damage by various forms of active oxygens and its inhibition by different scavengers using plasmid DNA. 783 95

Murine L1210 and human HL-60 leukemia cells grown for 5-7 days in medium containing 1% serum without selenium supplementation [Se(-) cells] were severely depressed in selenoperoxidase (SePX) activity relative to selenium-supplemented controls [Se(+) cells]. Catalase (CAT) activity in Se(-) cells was unaffected up to this point, but thereafter began to increase. Two manifestations of this increase have been differentiated for both cell lines: (a) short-term induction of CAT (up to approx. twofold) after 2-3 weeks, followed by (b) long-term selection for cells that irreversibly express much higher levels of CAT, e.g., > 100 times (L1210) and > 10 times (HL-60) the levels observed in Se(+) controls after approximately 20 weeks. Although superoxide dismutase, glutathione S-transferase, and glucose-6-P dehydrogenase activities were unchanged in Se(-) cells, GSH levels were elevated by 50-100%; like short-term CAT elevation, this could be reversed by supplying Se. Short-term Se(-) cells were more sensitive to H2O2-induced killing than Se(+) cells, evidently because SePX activity was important for peroxide detoxification. However, long-term Se(-) cells were markedly more resistant to H2O2 than Se(+) counterparts, consistent with the much higher levels of CAT in the former. Southern blot analysis revealed that the copy number of CAT DNA in a clone of long-term Se(-) L1210 cells was four- to fivefold greater than that in an Se(+) clone. Northern blot analysis of RNA from the same Se(-) clone showed a CAT mRNA level that was at least 40 times higher than that of the Se(+) control. Similar trends were observed for HL-60 cells. These results suggest that elevated CAT during long-term Se deprivation is a reflection of amplification and greater transcription of the CAT gene.
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PMID:Amplification and hyperexpression of the catalase gene in selenoperoxidase-deficient leukemia cells. 787 6

The relative importance of hydrogen peroxide generated as a consequence of irradiation with X-rays for the production of chromosomal aberrations has been studied in cultured CHO cells. Catalase introduced into cells by electroporation protected DNA from strand breakage induced by hydrogen peroxide given 4h later, and the yield of chromosome aberrations was also reduced. Nevertheless, when the cells were irradiated after treatment with catalase following a similar protocol and the yield of chromosomal aberrations analyzed at metaphase, no protective effect was observed as compared with cells treated with X-rays alone. These observations seem to support the hypothesis that hydroxyl radicals generated from hydrogen peroxide are not a major factor responsible for chromosome damage induced by ionizing radiation.
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PMID:Exogenous catalase introduced in CHO cells by electroporation does not protect against chromosome damage induced by ionizing radiation. 788 83

One way to study the effect of radiation on gene expression is to monitor changes in the levels of specific messenger RNAs. We describe the use of reverse transcription-polymerase chain reaction (RT-PCR) analysis, a faster and more sensitive procedure than the traditional techniques to monitor RNA levels. Using RT-PCR, we confirmed previous results showing increased levels of GADD45 transcripts after high dose-rate X-irradiation in normal human fibroblasts. No differences were observed in the transcript levels of beta-ACTIN, beta-MICROGLOBULIN, Cu-Zn SUPEROXIDE DISMUTASE (SOD-1) and CATALASE. In cells exposed to 3-6 Gy low dose-rate gamma-irradiation we observed increased levels of the GADD45 transcript and lower transcript levels of the genes TOPOISOMERASE II alpha, FACC, CYCLIN A and CYCLIN B. No differences were detected in the transcript levels of beta-ACTIN, beta-MICROGLOBULIN, SOD-1, URACYL-DNA GLYCOSYLASE, CYCLIN C, CYCLIN E, CYCLIN D1, CYCLIN D2, CYCLIN D3, TOPOISOMERASE I and TOPOISOMERASE II beta.
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PMID:Use of semiquantitative reverse transcription-polymerase chain reaction to study gene expression in normal human skin fibroblasts following low dose-rate irradiation. 788 81

Mild oxygenating agents generating low concentrations of hydrogen peroxide (H2O2) are effective alternatives to heat-activated 30% H2O2 in bleaching discolored, vital teeth. There are concerns about possible pathological effects of long-term exposure to bleaching agents, and irritation and ulceration of the gingiva and other oral soft tissues can occur. The objective of this study was to determine the effect of one of these agents on gingival fibroblasts in vitro. Microscopic examination revealed that concentrations of 0.05% to 0.025% of the agent appeared to kill most of the cells. At concentrations of 0.025% to 0.017% some morphological changes were noted; the cells appeared normal at concentrations of < or = 0.0125%. The agent significantly (P < or = 0.002) decreased proliferation (measured by incorporation of [3H]-thymidine into cellular DNA) at concentrations as low as 0.006%. The agent also had a dose-dependent effect on fibronectin production, measured by ELISA, causing significant (P < or = 0.03) decreases at concentrations as low as 0.017%. The agent significantly decreased the production of types I (P < or = 0.01) and III (P < or = 0.04) collagens (measured by ELISA) at concentrations as low as 0.0125%. Type V collagen was not detected under any conditions. Catalase, which catalizes the breakdown of H2O2, abolished toxic effects of a 0.05% solution. The results show that in vitro, the agent is toxic to human gingival fibroblasts, inhibiting several cellular functions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a bleaching agent on human gingival fibroblasts. 789 Dec 54

The extent of DNA damage and lipid peroxidation induced by kaempferol, a polyphenolic flavonoid with a molecular structure similar to quercetin, was studied under aerobic conditions in isolated rat-liver nuclei. Kaempferol induced significant (P < 0.05) concentration-dependent nuclear DNA degradation concurrent with lipid peroxidation; these effects were enhanced by iron(III) or copper(II). Catalase, superoxide dismutase (SOD), mannitol, and sodium azide did not show any inhibitory effect on the kaempferol-induced nuclear DNA damage in the presence of iron(III) or copper(II). On the other hand, all stimulated the kaempferol-induced DNA damage in the presence of iron(III); in the presence of copper(II) only SOD and mannitol showed statistically significant stimulatory effects. The kaempferol induced lipid peroxidation was significantly stimulated by catalase and sodium azide in the presence of iron(III). These results demonstrate the pro-oxidant properties of polyphenolic flavonoids, which are generally considered as antioxidants and anticarcinogens, suggesting their possible dual role in mutagenesis and carcinogenesis.
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PMID:Kaempferol-induced nuclear DNA damage and lipid peroxidation. 795 31


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