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 purpose of this investigation was to evaluate the effects of bacterial products derived from Pseudomonas aeruginosa on the function of airway cilia and to assess the role of phagocytes and oxygen radicals in the observed responses. Ciliary beat frequency (CBF) was measured in a perfusion chamber with a microscopic technique using tracheal epithelial cells obtained from normal sheep by brush biopsy (70% epithelial cells, 18% macrophages, 11% neutrophils). Baseline CBF ranged between 678 and 1,126 min-1. After 20 min of perfusion with the cell free supernatant of P. aeruginosa culture (mucoid strain), a concentration-dependent depression of CBF was observed with a 58% inhibition at a 1:1 dilution (P less than 0.05). The P. aeruginosa-derived products pyocyanin and 1-hydroxyphenazine also decreased CBF in a dose-related fashion. The cilion-inhibitory effects of the supernatant and bacterial products were markedly attenuated after centrifugation of the brush preparation (80% epithelial cells, 16.5% macrophages, 3.5% neutrophils). Glucose/glucose oxidase also caused a rapid, concentration-dependent cilioinhibition or ciliostasis. Catalase blocked or attenuated the ciliary effects of the supernatant, bacterial products and glucose/glucose oxidase. Thus bacterial products released from P. aeruginosa impaired ciliary activity by a pathway which involved neutrophils and was mediated by toxic oxygen radicals.
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PMID:Effects of P. aeruginosa-derived bacterial products on tracheal ciliary function: role of O2 radicals. 189 75

Reduced oxygen intermediates have been shown to directly depress cardiac muscle function at the subcellular, tissue, and whole animal levels. The exact species of reduced oxygen intermediate [superoxide anion radical (O2-.), H2O2, hydroxyl free radical (HO.)] and the concentrations necessary to depress cardiac muscle function have not been quantified. To better understand the role of O2-. and H2O2, we have studied rabbit right ventricular papillary muscle function in the presence of these reduced oxygen intermediates generated by a xanthine-xanthine oxidase system at 37 degrees C. In the presence of xanthine (0.1 mM) and xanthine oxidase (0.02 U/ml), 57.5 +/- 0.85 nmol.l-1.s-1 O2-. and 69.25 +/- 5.3 nmol.l-1.s-1 H2O2 were produced. In the presence of superoxide dismutase (SOD), O2-. was eliminated and H2O2 concentration increased. Catalase effectively eliminated the accumulation of H2O2 without significantly changing the rate of O2-. generation. When applied to isometrically contracting right ventricular papillary muscles, this system, with or without SOD and catalase, had no effect on peak developed tension or +/- dT/dt derived either from length-tension or force-frequency studies. However, when the xanthine oxidase concentration was increased to 0.112 U/ml, the rate of O2-. generation increased to 196.67 +/- 3.26 nmol.l-1.s-1 and H2O2 production increased to 142.19 +/- 9.3 nmol.l-1.s-1 with significant depression of papillary muscle tension development. SOD virtually eliminated O2-. production, whereas H2O2 production increased to 199.48 +/- 9.8 nmol.l-1.s-1 with no effect on papillary muscle tension development.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative identification of superoxide anion as a negative inotropic species. 283 94

The addition of the polyamines, spermine and spermidine, to human neutrophils caused a depression of the hexose-monophosphate (HMP) shunt activity of neutrophils stimulated with latex particles but not of unstimulated cells. The effect was dependent on the presence of bovine serum and was not observed when normal human serum was substituted for bovine serum. The polyamine oxidase (PAO) in bovine serum was probably responsible for generating the activity since normal human serum lacks PAO. A role for PAO was further supported by the finding that partially purified bovine PAO in the presence of polyamines similarly mediated inhibition of HMP shunt activity in stimulated neutrophils. Catalase failed to prevent the inhibitory effects of the PAO-polyamine system suggesting that H2O2 is not the responsible product. In addition, our results show that human pregnancy serum known to contain PAO activity in the presence of polyamines mediated a similar inhibition of the respiratory burst.
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PMID:Inhibition of the respiratory burst of human neutrophils by the polyamine oxidase-polyamine system. 309 15

Effects of exogenous antioxidant administration (0.5% and 2% ascorbate, beta-carotene and alpha-tocopherol in sucrose) on life-span, metabolic rate, activities of superoxide dismutase and catalase, levels of glutathione, inorganic peroxides and chloroform-soluble fluorescent material (lipofuscin) were examined in adult male houseflies. Administration of antioxidants at a level of 0.5% did not affect life-span, whereas, 2% ascorbate and alpha-tocopherol decreased average life-span. Metabolic rate of flies was unaffected, except by 2% ascorbate, which caused a decrease. Superoxide dismutase activity was depressed by 2% ascorbate at all ages, and by beta-carotene and alpha-tocopherol in older flies. Catalase activity was unaffected except by alpha-tocopherol at younger ages. Glutathione concentration was decreased by ascorbate and beta-carotene at both concentrations administered. Inorganic peroxides (H2O2) were increased by 2% beta-carotene and alpha-tocopherol. Only high concentrations of ascorbate and beta-carotene decreased the level of soluble fluorescent material. Results suggest that administration of exogenous antioxidants causes a compensatory depression of endogenous defenses.
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PMID:Effects of exogenous antioxidants on the levels of endogenous antioxidants, lipid-soluble fluorescent material and life span in the housefly, Musca domestica. 406 68

Catalase in extracts of the extreme halophile Halobacterium cutirubrum exhibits up to threefold stimulation by 0.5 to 1.5 m monovalent salts and by 0.1 m divalent salts. Above these concentrations, inhibition of enzyme activity is observed. The inhibitory effect, and to some extent the stimulation, is salt-specific; the effectiveness of a salt in inhibiting enzyme activity depends on both cation and anion. Thus, the order of effectiveness is MgCl(2) > LiCl > NaCl > KCl > NH(4)Cl, and LiCl > LiNO(3) > Li(2)SO(4). The magnitude of enzyme inhibition for the salts tested is positively correlated with their molar vapor pressure depression in aqueous solution. Stimulation of enzyme activity was observed when one salt was added at its optimal concentration in the presence of inhibiting concentrations of another salt, indicating that the effect on the enzyme is not due to changing water activity but probably to enzyme-salt interaction. Aqueous solutions of ethylene glycol, glycerol, and dimethyl sulfoxide containing no ions influence enzyme activity in the same manner as do salts.
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PMID:Effect of salts and organic solvents on the activity of Halobacterium cutirubrum catalase. 578 14

The mechanism of acute iron cardiotoxicity was investigated in isometrically contracting left atrial strips and right ventricular papillary muscles isolated from rabbit hearts. A 90-min exposure to iron (1.8 mM; as ferrous sulfate) reduced the peak-developed tension and the maximal rate of tension development. The presence of either N-acetylcysteine (20 mM), superoxide dismutase (2000 units/ml), or mannitol (5 mM) prevented this depression of contractility. Catalase (30,000 units/ml) was not protective against the effects of iron. Iron did not decrease myocardial adenosine triphosphate or creatine phosphate contents. The force-frequency relationship (positive staircase phenomenon) was examined in the absence and presence of iron. Iron did not reduce the positive inotropic response evoked by increasing the stimulation frequency, but at higher frequencies iron prolonged the time from peak tension to 90% relaxation. We conclude that acute iron cardiotoxicity may be mediated by free radical generation and does not involve impairment of myocardial high energy phosphate production.
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PMID:Depression of contractility in isolated rabbit myocardium following exposure to iron: role of free radicals. 669 79

Toxicosis due to paraquat, a redox cycling xenobiotic, is still a subject of much debate. In the present study on lipid peroxidation, paraquat had a biphasic effect on the malondialdehyde (MDA) level in rat liver microsomes; stimulation at the initial stage (within 10 min) and depression at the later stage. Although paraquat increased the initial rate of NADPH oxidation dose-dependently, the rate was not necessarily parallel with the increase in the MDA level. The MDA level increased linearly up to 0.1 mM paraquat added, but then it attained a plateau. The stimulation obtained by paraquat within 10 min was absolutely dependent on exogenous Fe2+ ion and NADPH, and the stimulation was entirely SOD sensitive, while the iron-driven increase in MDA was 20% sensitive. Thus, there were different mechanisms between iron-driven lipid peroxidation and paraquat-modified peroxidation. Catalase increased the level, but mannitol, a scavenger of OH, had no effect. EPR spectra showed that superoxide was formed dose-dependently up to 0.1 mM paraquat and that it attained a plateau at the same as MDA level described above. From these results, we concluded that paraquat stimulates lipid peroxidation through a mechanism dependent on the superoxide complex involving Fe2+ ion.
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PMID:Effect of paraquat on the malondialdehyde level in rat liver microsomes (in vitro). 802 66

Although in vitro studies have shown that oxygen free radicals depress the sarcolemmal Ca(2+)-pump activity and thereby may cause the occurrence of intracellular Ca2+ overload for the genesis of contractile failure, the exact relationship between changes in sarcolemmal Ca(2+)-pump activity and cardiac function due to these radicals is not clear. In this study we examined the effects of oxygen radicals on sarcolemmal Ca2+ uptake and Ca(2+)-stimulated ATPase activities as well as contractile force development by employing isolated rat heart preparations. When hearts were perfused with medium containing xanthine plus xanthine oxidase, the sarcolemmal Ca(2+)-stimulated ATPase activity and ATP-dependent Ca2+ accumulation were depressed within 1 min whereas the developed contractile force, rate of contraction and rate of relaxation were increased at 1 min and decreased over 3-20 min of perfusion. The resting tension started increasing at 2 min of perfusion with xanthine plus xanthine oxidase. Catalase showed protective effects against these alterations in heart function and sarcolemmal Ca(2+)-pump activities upon perfusion with xanthine plus xanthine oxidase whereas superoxide dismutase did not exert such effects. The combination of catalase and superoxide dismutase did not produce greater effects in comparison to catalase alone. These results are consistent with the view that the depression of heart sarcolemmal Ca2+ pump activities may result in myocardial dysfunction due to the formation of hydrogen peroxide and/or hydroxyl radicals upon perfusing the hearts with xanthine plus xanthine oxidase.
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PMID:Relationship between mechanical dysfunction and depression of sarcolemmal Ca(2+)-pump activity in hearts perfused with oxygen free radicals. 890 72

We have recently reported that in an anesthetized rat model, generation of oxygen free radicals (OFR) via i.v. administration of Xanthine plus Xanthine Oxidase [X + XO] resulted in death of about 90% of the animals within a 120-min observation period. Pretreatment of the rats with endogenous scavengers Superoxide Dismutase and Catalase, or with felodipine, a dihydropyridine calcium channel blocker, and/or with dopexamine, an agonist of beta 2 adrenoceptors as well as dopamine (DA-1) receptors significantly enhanced the survival rate to over 70%. The present study was designed to investigate whether lipid peroxidation and ensuing respiratory depression contributed to the lethal toxicity of the free radicals. In the control group, the death of the rats administered [X + XO] was proceeded by significant increases in the plasma lipid peroxides (PLP) and by a severe hypertensive response characteristic of an intense ischemic state, which was confirmed by the presence of hypercapnia, hypoxemia, and acidosis. Placement of the animals on the positive pressure ventilation prior to the administration of [X + XO] did not prevent increases in PLP but, prevented any adverse alterations in the respiratory markers and significantly enhanced survival rate up to 70%. In contrast, both felodipine as well as dopexamine prevented any increases in PLP, normalized blood gas profile, and significantly increased survival rate to 80 to 90%. These observations suggest that the lethal toxicity produced by oxygen free radical was due to respiratory distress. The relationship between increases in the PLP and respiratory depression and the mechanisms via which two pharmacologically distinct agents, felodipine and dopexamine, facilitated the salutary effects cannot be conclusively stated at this time. It is further suggested that although the doses of these two drugs employed in the present studies are not adequate to function as antioxidants, such a possibility cannot be entirely ruled out.
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PMID:Effect of pharmacological interventions in the prevention of lipid peroxidation and respiratory depression induced by oxygen free radicals in anesthetized rats. 890 25

Reactive free radical species appear to be involved in the ischemic injury of cardiac muscle, although the mechanisms by which oxygen-derived free radicals affect the heart cell function are not known. In the present study, cultured ventricular myocytes were exposed to an exogenous oxygen radical generating system. The myocyte-enriched, primary cultures were prepared from ventricles of new-born rat heart and exposed to a xanthine/xanthine oxidase (X+XO) system. The transmembrane potentials were recorded with glass microelectrodes. Cell contractions were monitored photometrically. The release of lactate dehydrogenase (LDH) in the medium was analysed. Quantitative measurement and the time course of the radical generation were performed by the electron paramagnetic resonance (EPR) spin trapping technique with the spin trap 5,5-dimethyl-1-pyroline-N-oxide (DMPO). We verified that X and XO alone had no significant functional and biochemical effects. The X+XO system produced a rapid decrease in the action potential amplitude. This effect was accompanied by a strong decrease in contractility and spontaneous rate. The time course of these functional defects were correlated with a progressive efflux of LDH from the cardiomyocytes. Prolonging the exposure to the X+XO system provoked the cessation of the spontaneous beatings and the progressive loss of the resting diastolic potential, together with a near total release of the cellular LDH. The LDH release and the functional depression were both efficiently prevented by catalase. On the contrary, superoxide dismutase (SOD) slowed down but did not protect against the functional and biochemical effects of the free radicals. In comparison, the EPR spectra obtained indicated that the X+XO system was associated with an important generation of superoxide anions but also with a small hydroxyl production. SOD scavenged the superoxide but a small .OH production persisted. Catalase (CAT) did not modify the superoxide generation but decreased the hydroxyl adduct formation. These results suggest that, although the generation of superoxide anions by the X+XO system was higher than the hydroxyl production, the functional injury and enzyme leakage seemed mainly mediated through a hydrogen peroxide-hydroxyl radical pathway. Cultured ventricular myocytes can be thus used as a valuable model to investigate the cellular mechanism of oxidant-induced damage in the heart.
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PMID:Correlation between direct ESR spectroscopic measurements and electromechanical and biochemical assessments of exogenous free radical injury in isolated rat cardiac myocytes. 943 21


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