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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extent of DNA damage and lipid peroxidation induced by myricetin, a polyphenolic flavonoid, were studied in isolated rat liver nuclei under aerobic conditions. Myricetin 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 inhibit myricetin-induced nuclear DNA damage in the presence of iron (III) or copper (II). However, all of these antioxidants stimulated myricetin-induced DNA damage in the presence of copper (II). Lipid peroxidation induced by myricetin was significantly inhibited only by SOD in the presence of copper (II), whereas it was enhanced 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 to be antioxidants and anticarcinogens, and suggest a dual role for these flavonoids in mutagenesis and carcinogenesis.
Cancer Lett 1993 Jun 15
PMID:Interactions of flavonoids, trace metals, and oxygen: nuclear DNA damage and lipid peroxidation induced by myricetin. 833 Mar 5

We studied the role of reactive oxygen intermediates (ROIs) in experimental liver metastasis induced in mice by the inoculation of COLON 26-M5 murine colon cancer cells, a highly metastatic variant of COLON 26 cells, and the effect of ROIs on the invasive capacity of the cells in an in vitro chemo-invasion assay model using reconstituted basement membrane matrigel. We also measured the release of ROIs from cells using electron spin resonance (ESR) spectrometry. Hydroxyl radicals (.OH) were constitutively released from the cells. This release was augmented by pre-treatment with phorbol 12-myristate 13-acetate (PMA). In experimental liver metastasis in CDF1 mice, the administration of recombinant human superoxide dismutase (r-hSOD) significantly increased the number of metastatic nodules, while administration of catalase significantly inhibited metastasis formation. In vitro pre-treatment of cells with PMA significantly increased the number of metastatic nodules. Invasive capacity of the cells was markedly augmented by pre-treatment with PMA. PMA-induced augmentation was significantly inhibited by the simultaneous addition of r-hSOD to the assay. Catalase had no significant effect. Our findings suggest that ROIs play an important role in tumor invasion and metastasis, and that hydrogen peroxide (H2O2) may contribute to the retention or extravasation of circulating tumor cells. Furthermore, the superoxide anion (O2-) released by tumor cells may play an important role in basement membrane degradation.
Int J Cancer 1993 Jul 30
PMID:Effect of reactive oxygen intermediates on the in vitro invasive capacity of tumor cells and liver metastasis in mice. 839 85

Bovine serum amine oxidase (BSAO, EC 1.4.3.6) catalyzes the oxidative deamination of polyamines giving rise to the corresponding aldehydes, ammonia and hydrogen peroxide (H2O2). This study demonstrates that amine oxidase (BSAO) purified from bovine serum and exogenous spermine caused cytotoxicity in Chinese hamster ovary (CHO) cells. Cytotoxicity occurred when cells were exposed to BSAO (0.0164-16.4 micrograms/ml) in the presence of spermine (1.9-340 microM). BSAO and spermine alone were not toxic at these concentrations. Cytotoxicity was dependent on the concentration of spermine and on the incubation time, and was also accelerated at 42 degrees C relative to 37 degrees C. Kinetic analysis of the enzymatic reaction, as a function of spermine concentration, showed Michaelis-Menten saturation kinetics. The apparent Vmax increased from 19.1 +/- 0.4 microM min-1 at 37 degrees C to 23.0 +/- 0.3 microM min-1 at 42 degrees C. The apparent Km decreased from 25.5 +/- 2.6 microM at 37 degrees C to 17.7 +/- 1.3 microM at 42 degrees C. Catalase inhibited cytotoxicity, suggesting that H2O2 was partially responsible for cytotoxicity. This work shows that the oxidation products of polyamines, rather than the polyamines themselves, are responsible for cytotoxicity in mammalian cells. The significance of this study is that amine oxidases could have therapeutic potential in cancer treatment regimens and a beneficial effect is likely when the enzyme is used together with clinical hyperthermia.
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PMID:Cytotoxicity and kinetic analysis of purified bovine serum amine oxidase in the presence of spermine in Chinese hamster ovary cells. 842 93

Delta-Aminolevulinic acid (ALA) is a heme precursor accumulated in lead poisoning and acute intermittent porphyria. ALA-induced DNA damage in the presence of metal ions was investigated with a DNA sequencing technique and a high-performance liquid chromatograph equipped with an electrochemical detector. ALA caused damage to DNA fragments obtained from c-Ha-ras proto-oncogene in the presence of Cu(II), but only slightly in the presence of Fe(II). ALA + Cu(II) induced piperidine-labile sites at thymine residues, especially in the 5'-GTC-3' and 5'-CTG-3' sequences of double-stranded DNA. Catalase and bathocuproine inhibited DNA damage induced by ALA + Cu(II). Typical .OH scavengers did not inhibit DNA damage, suggesting that active species other than .OH play a more important role in DNA damage. 8-Hydroxy-2'-deoxyguanosine formation by ALA increased with ALA concentration in the presence of Cu(II). Electron spin resonance studies using alpha-(1-oxy-4-pyridyl)-N-tert-butylnitrone as spin trap showed that carbon-centered radicals were generated during Cu(II)-catalyzed autoxidation of ALA. The major pathway of ALA autoxidation consists for the formation of 4,5-dioxovaleric acid and NH(4)+. Formation of a pyrazine derivative through ALA autocondensation was also observed. Concomitantly, O2- and H2O2 were generated during the Cu(II)-catalyzed ALA autoxidation. These results indicate that H2O2 reacts with Cu(I) to form a crypto-OH radical, such as the Cu(I)-peroxide complex, causing DNA damage. The possible mechanism for metal-dependent DNA damage by ALA is discussed in relation to the carcinogenicity of lead compounds and the increased frequency of liver cancer in acute intermittent porphyria.
Cancer Res 1996 Apr 15
PMID:Mechanism of oxidative DNA damage induced by delta-aminolevulinic acid in the presence of copper ion. 862 Apr 94

Benzene is a widely recognized human carcinogen. The mechanism of DNA damage induced by major benzene metabolites 1,4-benzoquinone (1,4-BQ) and hydroquinone (1,4-HQ) was investigated in relation to apoptosis and carcinogenesis. Pulsed-field gel electrophoresis showed that cellular DNA strand breakage was induced by benzene metabolites. Internucleosomal DNA fragmentation and morphological changes of apoptotic cells were observed at higher concentrations of benzene metabolites. Flow cytometry showed an increase of peroxides in cultured cells treated with benzene metabolites. 1,4-BQ induced these changes at a much lower concentration than 1,4-HQ. Damage to DNA fragments obtained from the c-Ha-ras-1 proto-oncogene was investigated by a DNA sequencing technique. 1,4-BQ + NADH and 1,4-HQ induced piperidine-labile sites frequently at thymine residues in the presence of Cu(II). Catalase and bathocuproine inhibited DNA damage, suggesting that H2O2 reacts with Cu(I) to produce active species causing DNA damage. Electron spin resonance studies showed that semiquinone radical was produced by NADH-mediated reduction of 1,4-BQ and autoxidation of 1,4-HQ, suggesting that benzene metabolites produce O2- and H2O2 via the formation of semiquinone radical. These results suggest that these benzene metabolites cause DNA damage through H2O2 generation in cells, preceding internucleosomal DNA fragmentation leading to apoptosis. The fates of the cells to apoptosis or mutation might be dependent on the intensity of DNA damage and the ability to repair DNA.
Cancer Res 1996 Nov 15
PMID:Oxidative DNA damage and apoptosis induced by benzene metabolites. 891 53

The antioxidant enzymes catalase, glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were determined in the androgen-response LNCaP and androgen-nonresponsive PC-3 and DU 145 cells as well as in prostatic epithelial cell cultures of benign and malignant human prostatic tissue. There were no differences between the enzyme activities of the human primary cell cultures from cancerous tissue and their normal counterparts. The enzyme activities of the three permanent cell lines were either higher (SOD, catalase, GR) or lower (GST, GPx) than in the primary cell cultures. In LNCaP cells catalase and GR were significantly higher, GST, in contrast, was significantly lower than in PC-3 and DU 145 cells. GST in PC-3 and DU 145 cells, and SOD in all the three cell lines showed no significant differences. Catalase, GPx and GR values were significantly different in the three permanent cell lines. The different enzymatic equipment of the prostate cancer cell lines provides the basis for experimental testing of new concepts of cancer treatment with the help of systematic modulations of the antioxidant defence systems in prostate cancer.
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PMID:Antioxidant enzymes in malignant prostate cell lines and in primary cultured prostatic cells. 916 5

The aim of the present study was to investigate the effects of biologically important catechols on the cytotoxicity of adriamycin, farmorubicin, and mitomycin C with respect to hydroxyl radical production. Catecholamines (adrenalin, noradrenaline, dopamine) and DOPA enhance the generation of hydroxyl radicals by chemotherapeutic antibiotics. Measures were done using a deoxyribose assay, in presence of the Co(II) + H2O2 system. Catalase and hydroxyl radical scavengers (mannitol, thiourea, cysteine, glutathione, L-lactic dehydrogenase) inhibited the deoxyribose damage caused by the drugs.
Cancer Detect Prev 1997
PMID:Effects of catechols on free radical formation by chemotherapeutic agents (adriamycin, farmorubicin, and mitomycin). 939 96

Environmental tobacco smoke (ETS) is a pervasive contaminant in the workplace. Our objective was to determine the oxidative stress effects of ETS on employees who are exposed. The results provide information that is useful to the resolution of risk assessment questions associated with ETS. We analyzed two blood draws from volunteers in our control and exposed groups. The level of exposure to ETS was determined through plasma cotinine measurements, which showed a 65% increase from the control group to the exposed group. Exposure to ETS resulted in a statistically significant increase of 63% of the oxidative DNA mutagen 8-hydroxy-2'-deoxyguanosine in the blood of exposed subjects. This oxidative DNA damage has been linked to an increased risk of developing several degenerative chronic diseases, including coronary heart disease and cancer. The exposed subjects also had increased levels of superoxide dismutase, catalase, glutathione peroxidase (GPOX), and glutathione reductase. However, these increases were only statistically significant in catalase and GPOX. Catalase levels were 13% higher in the exposed group, and GPOX levels were 37% higher in exposed volunteers. The biochemical evidence suggests that exposure to ETS causes oxidative stress, resulting in DNA damage that may increase the risk of certain diseases.
Cancer Epidemiol Biomarkers Prev 1998 Feb
PMID:Environmental tobacco smoke in the workplace induces oxidative stress in employees, including increased production of 8-hydroxy-2'-deoxyguanosine. 948 89

The study was carried out on 25 women with breast cancer, 25 with fibrocystic breast disease and 19 healthy subjects. Antioxidant enzyme activities and total antioxidant status (AOX) were measured in erythrocyte and plasma of patients and healthies. Among the studied parameters, the erythrocyte Glutathione Peroxidase (GSH-Px) and Catalase (CAT) activities of patients with breast cancer were significantly different as compared to the control group values (p < 0.002 and p < 0.001) respectively. There was no correlation between total antioxidant status and any of these enzymes in erythrocyte and plasma activities of subjects. However, the positive correlation was found between erythrocyte and plasma Superoxide Dismutase [SOD(CuZn)] activities in all groups. Our results indicate that enzymatic and nonenzymatic antioxidants are differentially altered in human breast tumors. Since the total antioxidant status measurement isn't sufficient to evaluate the oxidant damage in breast disease, antioxidant enzymes must be measured separately in order to get additional information.
Cancer Biochem Biophys 1998 Jun
PMID:Plasma and erythrocyte total antioxidant status in patients with benign and malign breast disease. 992 72

Chronic inflammation induced by Helicobacter pylori infection has been associated with an increased risk of stomach cancer. We have analysed 167 stomach biopsies from 99 patients for H. pylori infection and immunohistochemically for the expression of inducible nitric oxide synthase (iNOS), catalase and superoxide dismutases (SODs) as markers of oxidative stress. Biopsies were graded as follows on the basis of histology: normal, superficial gastritis, variable severity of atrophic gastritis with or without intestinal metaplasia, and dysplasia. iNOS was detected in inflammatory cells in all types of gastritis with or without H. pylori infection and independently of its severity. In foveolar cells, iNOS was observed in approximately 25% of all biopsies showing any type of gastritis, but in a markedly higher proportion of dysplastic samples. Catalase and Mn-type SOD in inflammatory cells and catalase in foveolar cells were more frequently observed in marked atrophic gastritis biopsies than in less severe gastritis. Individual differences were found in the expression of these enzymes within groups with the same severity of gastritis. Prolonged oxidative stress in severe gastritis and dysplasia may play an important role in gastric carcinogenesis, through increased damage of DNA and tissue by reactive oxygen and nitrogen species.
Eur J Cancer Prev 1998 Dec
PMID:Inducible nitric oxide synthase, anti-oxidant enzymes and Helicobacter pylori infection in gastritis and gastric precancerous lesions in humans. 992 91


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