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)

Injury to the gastrointestinal tract by oxygen dependent processes is important in ischemia, inflammatory bowel disease, and necrotizing enterocolitis. The Caco-2 cell line is an important tool in assessing various gastrointestinal functions and offers a unique opportunity to assess gastrointestinal oxidant metabolism on a cellular level. However, some Caco-2 cell functions change with time after confluence. To determine if antioxidant enzyme activity changes during differentiation, Caco-2 cells were grown to confluence, and superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities and specific mRNA content were quantitated. With time after confluence the enzymes demonstrated a small, but statistically significant increase in activity. Neither superoxide dismutase nor glutathione peroxidase mRNA levels correlated with enzyme activity changes. Catalase mRNA levels increased as catalase activity increased. Thus, differentiated Caco-2 cells express superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities and the superoxide dismutase, glutathione peroxidase, and catalase genes. Superoxide dismutase activity and glutathione peroxidase activity do not correlate with mRNA levels, and suggest that regulation may be at a level other than transcription. The correlation between catalase activity and catalase mRNA suggests differentiation may occur at transcription. If Caco-2 cells are used to elucidate oxidative metabolism, changes in activities of antioxidant enzymes as a function of cell differentiation should be considered.
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PMID:Antioxidant enzymes in the differentiated Caco-2 cell line. 142 66

Endogenous hydrogen peroxide (H2O2) release from aortic endothelial cells was studied in the presence of antioxidant enzyme inhibitors, mitochondrial inhibitors, a microsomal cytochrome P-450 inhibitor, and after oxidative stress induced with H2O2 or menadione. Extracellular H2O2 generation was determined spectrofluorometrically using 3-methoxy-4-hydroxy phenylacetic acid, and intracellular H2O2 production (in or near peroxisomes) was measured indirectly using aminotriazole, which inactivates catalase in the presence of H2O2. Extracellular H2O2 release was 0.079 +/- 0.005 nmol/min/mg protein in Hanks' balanced salt solution, was constant during a 120-min incubation period, and was not affected by the cell passage number. The half-life for catalase inactivation with aminotriazole was 23 min. Inhibition of catalase, glutathione reductase, or gamma-glutamylcysteine synthetase did not change the rate of extracellular release of H2O2. Furthermore, inhibition of the mitochondrial respiratory chain (rotenone, antimycin A) or microsomal cytochrome P-450 (8-methoxypsoralen) did not change extracellular H2O2 release or intracellular H2O2 production (at peroxisomes) by endothelial cells or cells in which glutathione reductase was inactivated. When the cells were exposed to exogenous H2O2 (30 microM), extracellular H2O2 was scavenged primarily by the glutathione redox pathway. Exogenously added H2O2 (100 microM) changed intracellular H2O2 production (in or near peroxisomes) only when the glutathione redox cycle was inactivated. Menadione (20 microM), which undergoes intracellular redox cycling, increased extracellular H2O2 release almost 4-fold to 0.3 nmol/min/mg protein. Furthermore, menadione increased peroxisomal H2O2 levels and decreased the half-life for catalase inactivation in the presence of aminotriazole to 13 min. Catalase inhibition increased extracellular H2O2 release during menadione treatment, indicating that H2O2 can diffuse across the plasma membrane during oxidant stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of hydrogen peroxide generation in cultured endothelial cells. 154 Mar 80

We used light microscopic immunohistochemistry to locate manganese superoxide dismutase, copper zinc superoxide dismutase, catalase, and glutathione-S-transferases in demineralized femora from rats of 4-14 weeks of age. Immunoblots confirmed the specificity of the polyclonal antibodies for the rat proteins of interest. Each of the enzymes exhibited a unique staining pattern. Copper-zinc superoxide dismutase was detected within some articular and epiphyseal chondrocytes of younger animals. Manganese superoxide dismutase was detected within some articular and epiphyseal chondrocytes, within some osteoprogenitor cells and osteoblasts, within many osteoclasts, and within some vascular smooth muscle cells. Catalase was identified within articular chondrocytes, epiphyseal chondrocytes, and osteocytes, whereas staining at the periphery of hypertrophic chondrocytes suggested extracellular and/or cell membrane-associted catalase. Glutathione-S-transferases were detected within and at the periphery of epiphyseal and articular chondrocytes and less prominently within cortical osteocytes. There were no major age-related changes in antioxidant enzyme distribution.
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PMID:Immunohistochemical identification of superoxide dismutases, catalase, and glutathione-S-transferases in rat femora. 157 Jul 63

Antioxidant enzyme levels were determined in kidneys during estrogen-induced cortical renal tumorigenesis in male Syrian hamsters. The activity of these enzymes in renal tumors were compared to those in the kidney cortex of untreated male castrated hamsters of different ages and in age-matched animals treated with diethylstilbestrol (DES) for varying periods. A transient increase in kidney Mn superoxide dismutase (MnSOD) and total SOD activity was seen after 1.5 and 3.1 months of DES treatment compared to untreated controls. However, after 4.4 months of DES exposure the activities of these antioxidant enzymes fell below untreated levels. The level of MnSOD and CuZnSOD was 3- to 10-fold lower compared to castrated male renal cortical values in DES-induced primary, serially transplanted and in autonomous renal tumour variants. Catalase activity declined steadily at 1.5 to 4.4 months of DES treatment. Low levels of catalase activity were found in all tumors examined. In general, Western blot analysis of immunoreactive proteins confirmed these findings, indicating that the low enzyme activities were due to low levels of enzyme proteins. Immunohistochemistry of the earliest tumor foci exhibited negligible antioxidant enzyme activity. The levels of these antioxidant enzymes were similar in all tumors surveyed, both primary and autonomous variants and in newborn kidneys, and they were about 10-fold lower than in normal kidney cortex or isolated proximal tubules.
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PMID:Superoxide dismutase and catalase levels during estrogen-induced renal tumorigenesis, in renal tumors and their autonomous variants in the Syrian hamster. 204 4

Evidence has been obtained that implicates the generation of reactive oxygen species as an early and critical event in the promotion of neoplastic transformation in mouse JB6 cells. The time courses for specific inhibition by CuZn-superoxide dismutase (CuZn-SOD) of the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced promotion of neoplastic transformation in JB6 cells and for changes in antioxidant enzyme activities associated with TPA-exposure were examined. The antipromoting effect of CuZn-SOD was found to be critically dependent on the time of addition of CuZn-SOD relative to the start of a 14-day exposure of cells to TPA. Treatment of JB6 P+ Clone 22 and Clone 41 cells with CuZn-SOD for 18 h before, simultaneously with or up to 1 h after exposure to TPA, all inhibited promotion of transformation maximally. Delay of addition of CuZn-SOD by 2 h or more after the start of TPA treatment resulted in a marked decrease in the promotion inhibitory effect. CuZn-SOD added 24 or 48 h after TPA had no effect on promotion of transformation. Exposure of JB6 cells to 0.2- (superoxide anion radical) generated exogenously by the aerobic xanthine oxidase reaction resulted in promotion of neoplastic transformation that was prevented by concurrent addition of CuZn-SOD. Taken together these studies provide evidence that increased superoxide anion generation within the first 2 h following TPA exposure is an essential event in promotion of transformation in JB6 cells. Upon TPA exposure, JB6 Clone 41 cells exhibited time-specific activity changes in the cellular SOD, glutathione peroxidase (GSH-Px), and catalase. SOD and GSH-Px activities were reduced to 54% and 26% respectively of basal levels within 2 h of TPA treatment. GSH-Px activity recovered to basal levels within 4 h and CuZn-SOD within 48 h. Catalase activity was maximally reduced to 50% of basal within 1 h after TPA treatment and rebounded to greater than basal levels within 4 h. It is postulated that a c-kinase-dependent event induces rapid elevation of superoxide anion following TPA exposure and that this leads to reduced activity of antioxidant enzymes. Since antipromotion by exogenous CuZn-SOD is effective only during the first 2 h following TPA exposure, this suggests that the promotion-relevant 0.2- elevation is transient.
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PMID:Early superoxide dismutase-sensitive event promotes neoplastic transformation in mouse epidermal JB6 cells. 282 3

The intracellular steady-state concentrations of hydrogen peroxide or superoxide anion were increased by inhibiting either catalase, glutathione peroxidase, or superoxide dismutase activities. Catalase was inhibited with aminotriazole while glutathione peroxidase activity was blocked by eliminating reduced glutathione after addition of either iodoacetamide diethylmaleate or phorone. The concentration of aminotriazole that stimulated chemiluminescence in 50% (60 mM) was very similar to the Ki for catalase activity (70 mM). Cyanide, an inhibitor of both catalase and superoxide dismutase, stimulated chemiluminescence in 50% at a concentration (0.15 mM) which is much closer from the Ki for superoxide dismutase (0.25 mM) than from the Ki for catalase (15 microM). The superoxide dismutase inhibitor diethyldithiocarbamate also increased chemiluminescence six- to ten-fold. Depletion of reduced glutathione stimulated spontaneous chemiluminescence when its concentration decreased below 4.5 mumol X g liver-1. The results shown herein suggest that the changes in the intracellular steady-state concentration occurring after inhibition of any antioxidant enzyme are responsible for the increased spontaneous chemiluminescence. Spontaneous chemiluminescence from intact cells may be used as a noninvasive method for monitoring intracellular free radical metabolism.
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PMID:Increased spontaneous chemiluminescence from liver homogenates and isolated hepatocytes upon inhibition of O2- and H2O2 utilization. 302 9

The growth of mycobacteria on perfluorodecalin-modified media was shown to be accompanied by distinct alterations in the activity of the antioxidant enzyme system in M. bovis BCG and M. lufu. In M. bovis BCG the levels of glutathione transferase and glutathione peroxidase-hydrogen peroxidase activity are decreased by 45.47% and 100.88%, respectively. In M. lufu, on the contrary, the level of superoxide dismutase is increased by 42.23%, with no changes observed in the levels of glutathione transferase and glutathione peroxidases. The data obtained suggest physiological heterogeneity of mycobacteria and, thus, open prospects for the differential approaches to the problem of increasing the efficacy of in vitro cultivation of various mycobacterial species, including M. leprae.
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PMID:[Functional characteristics of the antioxidative system in mycobacteria grown on perfluorodecalin-modified media]. 328 44

Exploratory factor analysis of reported specific activities of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase in normal human tissues, normal mouse tissues, vertebrate red blood cells and neoplastic human cell lines shows that the activities of copper-zinc superoxide dismutase, catalase and glutathione peroxidase in normal tissues are influenced by a single factor. Catalase activity has the highest loading and correlation with this factor, suggesting a catalase- or hydrogen peroxide-related influence. The activity of manganese superoxide dismutase is influenced by a separate factor. The activities of copper-zinc and manganese superoxide dismutases in normal tissues therefore appear to be dichotomously regulated. The activities of superoxide dismutase and glutathione peroxidase in vertebrate red blood cells are influenced by a single factor. The activity of catalase is influenced by a separate factor. The roles of glutathione peroxidase and catalase in hydrogen peroxide catabolism in red blood cells in fact differ. In neoplastic human cell lines, two bipolar factor factors appear to influence the activities of catalase and manganese superoxide dismutase, and glutathione peroxidase and copper-zinc superoxide dismutase, respectively. The factors are, however, mainly catalase and glutathione peroxidase activity factors as the loadings and correlations of manganese superoxide dismutase on the one hand and copper-zinc superoxide dismutase on the other, with the respective factors, are relatively small. Potentially low superoxide production and intrinsically low peroxidizability of tumour cell membranes underlie the peculiar variation of antioxidant enzyme activities in tumour cells. Factor analysis is proposed as a heuristic data reduction and hypothesis-creating technique for the variation of antioxidant and other functionally-linked enzyme activities in normal and pathological cells and tissues.
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PMID:Factor analysis of the activities of superoxide dismutase, catalase and glutathione peroxidase in normal tissues and neoplastic cell lines. 350 91

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

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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