Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The correlation between lipid peroxidation and morphologic changes was examined in Sprague-Dawley rat lungs after 30 Gy single thoracic radiation. The rats were sacrificed every week until the end of the fifth week after radiation. The left lungs were used for the measurement of lipid peroxides and antioxidant enzymes activities. The right lungs were examined by light and electron microscopy. Amounts of lung lipid peroxides were within normal limits, and no cellular degenerative changes were observed in the lungs except for subendothelial and interstitial edema 2 weeks after radiation. Lipid peroxides drastically increased and marked degenerative cellular changes such as edematous swelling, vacuolation, and destruction of cell membranes occurred in the alveolar septa following the third week after radiation. The activities of catalase were significantly higher during the period from the second to the fifth week and those of superoxide dismutase and glutathione peroxidase increased at the end of the fifth week. Our results demonstrated that the acceleration of lipid peroxidation was well correlated with the morphologic expression of cell injury in the irradiated lungs.
Exp Mol Pathol 1989 Apr
PMID:Correlation among lung damage after radiation, amount of lipid peroxides, and antioxidant enzyme activities. 270 87

Resonance Raman spectra are reported for catalases from bovine liver, the ascomycete fungus Aspergillus niger, and the bacterium Micrococcus luteus. The vibrational frequencies of the oxidation-, spin-, and coordination number-sensitive spectral bands are indicative of high spin pentacoordinate hemes in the resting ferric enzymes of each of these organisms. This result is in accord with the crystal structure of bovine catalase (Fita, I., and Rossmann, M.G. (1985) J. Mol. Biol. 185, 21-37). In contrast, the crystallographic study of catalase from the ascomycete Penicillium vitale (Vainshtein, B. K., Melik-Adamyan, W. R., Barynin, V. V., Vagin, A.A., Grebenko, A. I., Borisov, V. V., Bartels, K. S., Fita, I., and Rossmann, M. G. (1986) J. Mol. Biol. 188, 49-61) showed electron density on the distal side of the heme which could imply the presence of a sixth ligand, possibly a water molecule. However, both of these crystallographic studies showed the proximal ligand in catalase to be a tyrosine. The present study confirms tyrosinate coordination in each of the three catalases from the appearance of selected resonance-enhanced tyrosine vibrational modes. The most characteristic band is the tyrosinate ring mode at approximately 1612 cm-1 which is maximally enhanced with 488.0 nm excitation. The appearance of tyrosinate modes at 1607 and 1245 cm-1 in the resonance Raman spectra of M. luteus cyano catalase serves to identify tyrosine as an axial ligand in bacterial as well as eukaryotic catalases. Unlike non-heme iron tyrosinate proteins, whose resonance Raman spectra are dominated by several intense bands diagnostic of tyrosine ligation, the heme-linked tyrosine modes are not easily distinguished from the large number of porphyrin vibrations.
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PMID:Comparative spectral analysis of mammalian, fungal, and bacterial catalases. Resonance Raman evidence for iron-tyrosinate coordination. 275 85

The interaction of mouse liver catalase with subcellular membranes was studied, and an ionic interaction with a variety of membranes, including those derived from the microsomes, was observed. The interaction with microsomal membranes was found to be abolished by pre-treatment of catalase with neuraminidase, indicating a functional significance for catalase-bound sialic acid. Catalase activity was found to be enhanced when bound to membranes, and evidence for a weak association of catalase with peroxisomal structure in mouse liver was also obtained. It is concluded that mouse liver catalase has a capacity to bind to a variety of subcellular membranes in vivo and that this interaction may be consistent with a general protective role for the enzyme, as well as being compatible with a model of peroxisomal biogenesis which involves the interaction of catalase with microsomal membranes.
Mol Cell Biochem 1989 Mar 16
PMID:On the interactions of catalase with subcellular structure. 275 57

Since the chronically cyanotic tetralogy of Fallot (TOF) myocardium is more sensitive to reperfusion injury after cardiac surgery than the adult myocardium, we decided to study the regulation of myocardial superoxide dismutase (SOD), catalase and glutathione peroxidase by oxygen tension. TOF myocytes were cultured at a Po2 of 150 mmHg for 30 days to establish the culture. The cells were then cultured at Po2 of 150 and 40 mmHg and the myocyte antioxidant enzymes measured at days 3, 7, 14 and 21. On day 21 the myocytes cultured at Po2 of 40 mmHg were then cultured at 150 mmHg and SOD and catalase activities measured on days 28 and 35. Although there were no differences in the rates of incorporation of 35S-methionine into the myocytes at either Po2 on these days, the myocytes scavenger enzyme levels were significantly higher by day 14 when cultured at a Po2 of 150 mmHg than at a Po2 of 40 mmHg. With the increase in oxygen tension from 40 to 150 mmHg, SOD and catalase activities increased significantly by day 35. The myocytes cultured at Po2 40 mmHg were more sensitive by day 7 to an hypoxanthine-xanthine oxidase generated free radical injury than the Po2 150 mmHg cultured cells. The regulation of these enzyme activities by oxygen tension and the increased sensitivity to free radical injury of the myocytes cultured at an oxygen tension of 40 mmHg provide putative evidence that the chronically cyanotic myocardium may be less well protected than the normally perfused myocardium against oxygen-mediated free radical injury and be at higher risk for cardiovascular surgery.
J Mol Cell Cardiol 1989 Jun
PMID:Effect of oxygen tension on the anti-oxidant enzyme activities of tetralogy of Fallot ventricular myocytes. 277 8

Because oxidative processes can participate in tumor promotion, it is likely that the cellular antioxidant defense also plays a role. We have compared the levels of the three major antioxidant enzymes, Cu,Zn-superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx), in promotable mouse epidermal JB6 cells clone 41 and nonpromotable cells, clone 30. We found that the constitutive activities of SOD and catalase were approximately twice as high in clone 41 as in clone 30 while the GPx activities were comparable. Correspondingly, catalase protein concentrations were higher in clone 41, according to immunoblots. Northern blot analysis indicated that the steady-state mRNA concentrations for SOD and catalase, but not for GPx, were considerably higher in clone 41 than in clone 30. Southern blot analysis showed no difference between the two clones in their complements of the SOD and catalase genes. Clone 41 also contained slightly higher constitutive levels of glutathione. The higher antioxidant capacity of promotable clone 41 may protect it from excessive toxicity of oxidant promoters and allow growth stimulation. Certain tumor promoters that lack oxidizing properties may generate a cellular prooxidant state by a variety of mechanisms (e.g., it had been reported that the phorbol ester PMA decreases the activities of catalase and SOD in mouse skin). We found for JB6 cells that this loss of enzyme activity was due to a decrease in the steady-state concentrations of catalase and SOD mRNA. No significant changes in the rates of transcription were detected in nuclear run-off experiments. The observed decreases in catalase and SOD can be considered as part of the complex reprogramming of gene expression that is set in motion by phorbol-12-myristate-13-acetate.
Mol Carcinog 1989
PMID:Constitutive and phorbol-myristate-acetate regulated antioxidant defense of mouse epidermal JB6 cells. 278 90

Ischemia-reperfusion activates polymorphonuclear leukocytes (PMN). Depletion of PMN has been shown to reduce the size of experimental myocardial infarction. We have studied whether PMN activated by phorbol myristate acetate (PMA) would depress function of the isolated rat heart, and if this effect was mediated by oxygen free radicals (OFR). Cells and/or drugs were added to the perfusate into the aortic cannula for 10 min, followed by a 30 min recovery period. Oxygen free radicals formation was verified by chemiluminescence (CL). PMA-activated PMN (n = 13) caused CL response of 27,493 +/- 5113 counts (mean +/- S.E.M.) and reduced left ventricular developed pressure (LVDP) to 30 +/- 9% and coronary flow (CF) to 49 +/- 7% of the baseline value at the end of the observation period. Addition of super-oxide dismutase (SOD) and catalase (CAT) (n = 11) reduced the CL response to 5623 +/- 806 counts, but did not influence either LVDP (36 +/- 15%) or CF (51 +/- 18%). Addition of thiourea (TU) to the activated cell suspension (n = 8) further reduced the CL response (3663 +/- 474 counts), and LVDP was 86 +/- 5% and CF was 87 +/- 3%. When TU + SOD + CAT was mixed with PMN + PMA (n = 11), the CL was almost abolished (117 +/- 21 counts) and LVDP was 73 +/- 8% and CF was 94 +/- 6%. When CF was reduced (n = 7) alike the CF reduction in the hearts receiving PMA + PMA, LVDP was not significantly changed at the end of the observation period (75 +/- 6%). Unactivated PMN (n = 8) caused minor response of LVDP and CF, similar to PMN + PMA + TU and PMN + PMA + SOD + CAT + TU. PMA alone (n = 8) was cardiotoxic and caused changes similar to PMN + PMA. This effect was not inhibited by scavengers (n = 6). The supernatant of the PMN + PMA suspension (n = 7) did not impair cardiac function, suggesting that no free PMA was available after mixing with PMN. We conclude that activated PMN in the coronary circulation depressed cardiac function and increased vascular resistance due to OFR production.
J Mol Cell Cardiol 1989 Sep
PMID:Functional impairment in isolated rat hearts induced by activated leukocytes: protective effect of oxygen free radical scavengers. 281 Mar 77

The results of our experiments demonstrated that one hour of ischemia followed by one hour of reflow in the kidney caused a reduction in (Na+K+)ATPase activity and microsomal sulfhydryl content as well as an increase in microsomal lipid peroxidation. Renal venous malondialdehyde concentration was increased soon after reperfusion of the ischemic kidney. All these changes were rectified by an infusion of 0.123 mmol N-(2-mercaptopropionyl)glycine/kg over a 70 min period. On the other hand, an in vitro addition of 0.01-0.5 mM N-(2-mercaptopropionyl)glycine to a membrane preparation in the presence of H2O2 and Fe3+ did not prevent but rather potentiated the free radical effect on the enzyme activity. However, addition of superoxide dismutase alone or with catalase together with 2-MPG were effective in preventing the enzyme depression induced by H2O2. The results therefore indicate that free radical generation participates in the evolution of ischemia/reperfusion cell injury and thiol-reducing agents may be beneficial in alleviating the cell damage in vivo.
Mol Cell Biochem 1987 Dec
PMID:Effects of N-(2-mercaptopropionyl)glycine on ischemic-reperfused dog kidney in vivo and membrane preparation in vitro. 283 50

The direct effect of oxygen metabolites was studied on isolated perfused rat hearts. Superoxide anion (O2-.) and hydrogen peroxide (H2O2) were generated by adding purine (2.3 mM) and purified xanthine oxidase (0.06 U/ml) to Krebs-Henseleit buffer (pH 7.4). Xanthine oxidase was added to the purine-containing perfusate either near the aorta (group A, which gave H2O2 less than 10 microM) or at a distant point from the aorta (group B, which gave 250 to 300 microM H2O2). The generation rate of O2-. was 31.7 +/- 1.0 nmol/ml/min in the experimental conditions. Contractile function, tissue adenosine triphosphate (ATP), and ultrastructure were not affected in group A. In contrast, hearts in group B showed marked decrease in contractility (+dP/dt) to 24.4 +/- 4.3% of control values. ATP levels were also markedly reduced from control values of 23.4 +/- 0.7 to 7.4 +/- 0.7 mumol/g dry tissue. Ultrastructure in group B hearts revealed "wavy" and disintegrated sarcolemma, depletion of glycogen deposits, and swelling and disruption of mitochondria. Release of the thiobarbituric acid reactive products including malondialdehyde was significant in the effluent (1.68 +/- 0.17 nmol/min/g wet tissue). These changes were almost completely prevented by catalase, but not by superoxide dismutase and deferoxamine. Moreover, exogenous H2O2 perfusion (300 microM) showed results similar to group B hearts. These observations suggest that H2O2 plays a major role in the injury. O2- does not appear to damage hearts directly, although it is important as a precursor of H2O2 and other radical species including hydroxyl radical.
J Mol Cell Cardiol 1988 Nov
PMID:Myocardial dysfunction and ultrastructural alterations mediated by oxygen metabolites. 285 30

Guinea pig glomeruli were grown for 22 days in a serum-free medium composed of Waymouth's MB 752/1 supplemented with sodium pyruvate, nonessential amino acids, and antibiotics. To this basic medium was added insulin, transferrin, selenium (Se), tri-iodothyronine, or fibronectin (FN) - either singly, or in various combinations - and sequential quantitative studies of the glomerular outgrowths were performed. Total cells in glomerular outgrowths, mitotic index, and glomerular attachment rate were determined and compared with values for glomerular outgrowths in media containing either no additions or all of the above components. FN was required for whole glomerular attachment, while transferrin plus FN was required for mitosis in glomerular cell outgrowths. Insulin and tri-iodothyronine slightly increased glomerular cell outgrowth by slightly increasing whole glomerular attachment, but had little effect on mitosis in glomerular outgrowths. The effect of Se was complex. Se did not affect whole glomerular attachment or mitosis in the presence of transferrin plus FN. However, in a medium containing transferrin, FN, and 3-amino-1,2,4-triazole (AT) (an inhibitor of catalase and glutathione peroxidase), Se increased total cell number but had little effect on the glomerular attachment rate or the mitotic index. Morphologic analysis of glomeruli early in culture suggested that Se may act by decreasing the amount of or delaying the time of cell death. In all of the media tested, total DNA was relatively constant over the course of 22 days, suggesting the possibility that glomerular cells cultured in a serum-free medium are part of a cell renewal system.
Virchows Arch B Cell Pathol Incl Mol Pathol 1986
PMID:Kidney glomerular explants in serum-free media: role of individual medium components in cell outgrowth. 287 79

The effects of oxygen-derived radical scavengers (ODRS) on the heart was investigated during the calcium paradox. Perfusion with Ca2+-free medium caused cell separation at the intercalated discs and changes in the endothelial cells. Upon Ca2+ reintroduction, a massive cell damage occurred. The cytosolic enzyme, creatine phosphokinase (CPK), was released in large amounts (p less than 0.001). The tissue adenosine triphosphate (ATP) was reduced to 3.7 mumol/g dry weight from the control value of 21.6 mumol/g dry weight and tissue Ca2+ content was increased threefold. The treatment with superoxide dismutase (SOD) and catalase (CAT) increased percentage of normal cells (62.2%) compared to nontreated Ca2+ paradox group (0.2%) and caused negligible leakage of CPK. Tissue ATP was preserved (p less than 0.03), and Ca2+ content was also reduced in the hearts treated with SOD and CAT (p less than 0.03). The cell membranes and vascular endothelium were well preserved in the hearts treated with SOD and CAT. Boiled SOD and CAT administered were totally ineffective. It is suggested that oxygen-active species may have a role in the Ca2+ paradox injury.
Virchows Arch B Cell Pathol Incl Mol Pathol 1987
PMID:Oxygen derived radicals related injury in the heart during calcium paradox. 289 1


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