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)

In aerated water solutions Fe(II)Cytochrome c is slowly oxidized to Fe(III)Cytochrome c by molecular oxygen, from which superoxide anion radicals are produced (kobs = 2.7 x 10(-4) min-1 at 37 degrees C and pH = 7.3). The biological importance of this reaction has been evidenced by kinetic investigations in the presence of scavengers. In the presence of Superoxide dismutase the oxidation rate is strongly enhanced (kobs = 3 x 10(-3) min-1 at 37 degrees C). Catalase and mannitol reduce the rate constant values by 50% and 25% respectively either in the presence or in the absence of Superoxide dismutase: differences between rate constants correspond to the differences in stoichiometric redox ratios indicating that hydrogen peroxide and hydroxyl radicals are formed subsequently to the production of superoxide anion radicals.
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PMID:Production of reactive oxygen-derived species by redox reactions between Fe(II)cytochrome c and oxygen. A kinetic study. 762 18

The present study intends to define the role of the endothelium derived relaxing factor nitric-oxide (EDRF-NO) and the reactive oxygen intermediates in hypersensitivity to 5-hydroxytryptamine (5-HT) observed in abdominal aorta rings of two kidney-two clip hypertensive rats. Methylene Blue (which blocks production of cGMP by EDRF-NO) and Nw-nitro-L-arginine (which inhibits EDRF-NO synthesis), both shifted 5-HT dose-response curves to the left and completely abolished the differences in sensitivity to the agonist. The aortic perfusion with Krebs-Alcohol 20% (v/v) suppressed vascular relaxation to Ach (10(-5) M) and also abolished differences in sensitivity to 5-HT. These results suggest that a lower availability of EDRF-NO accounts for a higher 5-HT sensitivity in vessels of hypertensive rats. On the contrary, ridogrel (inhibitor of tromboxane-synthase and blocker of PGH2 and TxA2 receptors) did not suppress the hypersensitivity to 5-HT. In addition, since the superoxide anion (O2-) inactivates EDRF-NO, the effects of Superoxide dismutase (SOD) and Catalase (CAT) added in the bath were analyzed. Significant changes in sensitivity (P < 0.005) were found only for vessels of hypertensive rats (SOD depressing and CAT increasing sensitivity to 5-HT). Complementary, SOD activity was evaluated in the aorta homogenates and was found to be significantly lower in the hypertensive rats [(differences between hypertensive and sham rats, mU.mg wet weight tissue-1: 7 days after clipping, -183 +/- 67 (n = 11), P < 0.02; 21 days, -160 +/- 70 (n = 9), p < 0.05]. Results would indicate: 1. Lower EDRF-NO availability in vessels of the hypertensive animals which would account for higher sensitivity to 5-HT; 2. Such a lower EDRF-NO might depend, in part, upon its greater inactivation by O2- anions; 3. A greater presence of O2- anions in the vessels of hipertensive rats that might be favored by the lower SOD activity concentration in the vascular wall.
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PMID:Nitric oxide and superoxide anions in vascular reactivity of renovascular hypertensive rats. 765 50

NADPH-quinone reductase catalyzes the two-electron reduction of quinones such as menadione, and generally is considered to play a protective role against quinone-mediated toxicity. Recent studies have shown that reactive oxygen intermediates may be produced during metabolism of quinones by quinone reductase. Experiments were carried out to evaluate the effect of iron complexes on production of hydroxyl radical (.OH) when menadione was oxidized by a rat liver cytosolic fraction. Menadione-stimulated H2O2 production when added to the cytosol; dicoumarol, a potent inhibitor of quinone reductase, completely blocked this stimulation. Results were identical with either NADH or NADPH as reductant. In the absence of added iron, .OH, assessed as oxidation of chemical scavengers, was not produced. Various ferric chelates, added to the cytosol in the absence of menadione, did not catalyze .OH production. However, .OH was produced in the presence of menadione with all ferric complexes evaluated except for ferric-desferrioxamine. Catalase, competitive scavengers and GSH inhibited .OH production, as did dicoumarol. Superoxide dismutase inhibited with ferric-ATP, ferric-citrate, ferric-histidine or ferric ammonium sulfate as iron catalysts, but had no effect with ferric-EDTA or ferric-diethylenetriamine penta-acetic acid. Reduction of the ferric complexes was increased by menadione. NADH and NADPH were equally effective as cofactor for all these reactions. Metabolism of menadione in the presence of iron complexes caused inactivation of enzymes present in the cytosolic fraction such as glutamine synthetase and lactic dehydrogenase. These results indicate that metabolism of menadione by quinone reductase can lead to the production of .OH in the presence of various ferric catalysts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Requirement for iron for the production of hydroxyl radicals by rat liver quinone reductase. 769 Apr

Effects of hypoxia-reoxygenation (H-R) on myocytes isolated from 10 week hypertrophied and sham control rat hearts were studied. Myocyte hypertrophy was indicated by an increase in cell size. Superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) enzyme activities were significantly higher and lipid peroxidation (TBARS) was lower in hypertrophied myocytes prior to any H-R. Hypertrophied myocyte population showed significantly less damage to cell morphology due to H-R. In sham as well as hypertrophied myocytes, Na+ and Ca2+ contents were increased by H-R, but Ca2+ accumulation was significantly less in the hypertrophied myocytes. Both SOD and GSHPx activities were depressed by the oxidative stress in the sham myocytes whereas these activities were not significantly changed in the hypertrophied myocytes. Catalase activity in the prehypoxic sham and hypertrophied myocytes was comparable and this activity did not change during H-R. There was a significant increase in lipid peroxidation due to H-R but this change was less in hypertrophied myocytes. This study shows less vulnerability of hypertrophied myocytes to oxidative stress and an increase in endogenous antioxidant reserve may have an important role in mediating this protection.
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PMID:Endogenous antioxidants in isolated hypertrophied cardiac myocytes and hypoxia-reoxygenation injury. 776 Mar 50

Previous work in our laboratory has shown the relation between leukocytes (WBC) and the generation of oxidants in endotoxin (LPS) shock. The purpose of this study was to find out if WBC-derived oxidants can produce acute lung injury in guinea pigs given LPS. We alos evaluated the efficacies of steroids and antioxidants against the initial changes in LPS-induced lung injury. One group of guinea pigs (200-250 g, male) received 0.7 mg/kg (LD50, 24 hrs.) of E. coli LPS in the peritoneal cavity (group I). The animals in group II received 30 mg/kg of methylprednisolone (MP), followed by intraperitoneal LPS. The animals in group III were given 30 mg/kg of 2-aminomethyl-4-tert-butyl-6-propionylphenol hydrochloride (ONO-3144), a known as antioxidant (OH radical scavenger), and then an injection of LPS. The animals were killed at following time course: 30, 60 or 180 minutes after the LPS injection. Hematological examinations (WBC counts), total cell counts and differential counts in bronchoalveolar lavage (BAL) fluid were done along with light microscopic studies. Superoxide dismutase (SOD) activity, catalase activity and malonaldehyde (MDA) produced as a result of lipid peroxidation in the lung were measured and correlated with histological changes. Survival ratios of the three groups were compared. The results obtained were: 1) Significant leukopenia occurred in all groups. 2) In group I, WBC, especially eosinophils, were recovered by BAL and the total cell number of the BAL fluid had increased by 180 minutes after LPS injection, but MP or ONO-3144 treatment inhibited the migration of WBC (eosinophils and neutrophils) into alveolar lumen after LPS injection. 3) Histologic examinations revealed diffuse edema, hemorrhage, and marked leukocyte infiltration in the alveoli in group I, but not in group II or III. 4) SOD activity in all group diminished below the control level. Catalase activity had significantly increased by 180 minutes after LPS injection in group I, but not in group II or III. MDA had increased remarkably by 60 minutes after injection of LPS in group I, but MP or ONO-3144 treatment prevented such increases. 5) Animals in group II and III survived significantly longer than those in the other group. In conclusion, these findings suggest that LPS provokes WBC-mediated vascular damage in the lung and steroids or antioxidants can minimize the injury and prevent edema formation. Steroids might be useful for achieving quantifiable changes in LPS-induced WBC chemotaxis to the lung and for decreasing oxidant-induced lung injury.
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PMID:[Endotoxin-induced lung injury. The roles of leukocytes and oxidants, and the efficacies of steroids and antioxidants]. 777 52

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

The reactivity and toxicity of nitric oxide is modest in comparison to oxidants derived from nitric oxide. Exposure of Escherichia coli to 1 mM nitric oxide under aerobic or anaerobic conditions did not decrease viability of the bacteria. Peroxynitrite (1 mM), the reaction product of superoxide and nitric oxide, was completely bactericidal after 5 s. The nitrovasodilator, 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1), slowly decomposes to release both nitric oxide and superoxide and thereby produces peroxynitrite. SIN-1 killed E. coli in direct proportion to its concentration with an LD50 of 0.5 mM. Copper, zinc superoxide dismutase (50-400 units/ml) provided substantial but not complete protection against SIN-1 killing. Catalase (500-10,000 units/ml) partially protected in direct proportion to its concentration, while inactivated catalase was not protective. Superoxide dismutase and catalase together completely protected E. coli against SIN-1 toxicity. Oxy-hemoglobin eliminated both SIN-1 and peroxynitrite toxicity. The bactericidal activity of SIN-1 was further enhanced by pterin plus xanthine oxidase. Pterin plus xanthine oxidase alone or together with Fe3+ ethylenediamine tetraacetate produced no significant decrease in E. coli viability. Hydrogen peroxide was not directly toxic to the bacteria, but E. coli pretreated with hydrogen peroxide were more susceptible to peroxynitrite, SIN-1, and the aerobic oxidation products of nitric oxide. Hydrogen peroxide pretreatment did not increase significantly the toxicity of nitric oxide under anaerobic conditions. Our results suggest that peroxynitrite is far more toxic to E. coli than nitric oxide or its by products from aerobic oxidation.
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PMID:The comparative toxicity of nitric oxide and peroxynitrite to Escherichia coli. 784 Jun 33

In previous studies we have found that a single acute dose of ultraviolet radiation to murine skin causes a large degree of destruction of enzymic and non-enzymic antioxidants immediately after irradiation. In the present study, we wished to elucidate the recovery of antioxidants after a single dose of ultraviolet (UV) radiation. We measured antioxidants and lipid hydroperoxides (as a marker of membrane damage) in murine epidermis and the dermis at 0, 3, 12, 24, 72 and 120 h after exposure to UV radiation (25 J/cm2, UVA+UVB). Lipid hydroperoxides showed the highest values immediately after UV exposure and returned to control values within 24 h in both epidermis and dermis. The activities of catalase, glutathione peroxidase and glutathione reductase showed the lowest activities immediately after UV exposure; superoxide dismutase activities reached a minimum at 3 h postexposure. The pattern of recovery was different for each enzyme and for epidermis and dermis. The activities of superoxide dismutase and catalase decreased remarkably and recovered slowly. Superoxide dismutase in the dermis recovered full activity by 120 h and in the epidermis by 12 h. Catalase activity in both epidermis and dermis had returned to only 50% of control activity at 120 h, although the epidermis showed a temporary increase (to 93%) at 24 h. Glutathione peroxidase and glutathione reductase were slightly decreased immediately after irradiation, recovered to 100% at 3 h and then increased to 200-250% in both the epidermis and the dermis at various times; values had returned to 100% in epidermis by 120 h but remained elevated in dermis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recovery of antioxidants and reduction in lipid hydroperoxides in murine epidermis and dermis after acute ultraviolet radiation exposure. 788 Jul 56

Repeated ischemic insults at one hour intervals result in more severe neuronal damage than a single similar duration insult. The mechanism for the more severe damage with repetitive ischemia is not fully understood. We hypothesized that the prolonged reperfusion periods between the relatively short ischemic insults may result in a pronounced generation of oxygen free radicals (OFRs). In this study, we tested the protective effects of superoxide dismutase (SOD) and catalase (alone or in combination), and U78517F in a gerbil model of repetitive ischemia. Three episodes (two min each) of bilateral carotid occlusion were used at one hour intervals to produce repetitive ischemia. Superoxide dismutase and catalase were infused via osmotic pumps into the lateral ventricles. Two doses of U78517F were given three times per animal, one half hour prior to each occlusion. Neuronal damage was assessed 7 days later in several brain regions using the silver staining technique. The Mann-Whitney U test was used for statistical comparison. Superoxide dismutase showed significant protection in the hippocampus (CA4), striatum, thalamus and the medial geniculate nucleus (MGN). Catalase showed significant protection in the striatum, hippocampus, thalamus, and MGN and the substantia nigra reticulata. Combination of the two resulted in additional protection in the cerebral cortex. Compared to the controls, there was little protection in a dose of 3 mg/kg of U78517F. There was significant protection with a dose of 10 mg/kg in the hippocampus (CA4), striatum, thalamus, medial geniculate nucleus and the substantia nigra reticulata.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Superoxide dismutase, catalase, and U78517F attenuate neuronal damage in gerbils with repeated brief ischemic insults. 806 23

Aortic rings, 4 mm in length, were obtained from rats and placed on isometric force transducers in oxygenated Krebs buffer. Following a period of stabilization, the cumulative dose response relationship to norepinephrine was assessed. The vessels were washed and allowed to return to baseline in Krebs buffer containing xanthine (0.5 mM). Xanthine oxidase (0.1 U/ml) was then added to the bath and vessels incubated for 30 min. The vessels were resuspended in Krebs buffer and cumulative dose-response curves to norepinephrine reevaluated. The results indicate that generation of reactive oxygen metabolites by xanthine/xanthine oxidase decreases the pD2 from 7.80 +/- 0.04 to 7.40 +/- 0.09 with the endothelium intact. Removal of the endothelium did not attenuate the contractile dysfunction, indicating that endothelial-derived metabolites were not mediating the loss of vasoconstrictor effectiveness. Maximal tension development did not differ between normal and oxidized vessel rings. Introduction of oxypurinol (0.2 mg/ml) to the bath prevented the loss of constrictor responsiveness, thereby confirming that all of the oxidants were derived from the xanthine/xanthine oxidase reaction. Superoxide dismutase (200 U/ml) partially prevented the loss of norepinephrine responsiveness produced by xanthine oxidase-derived radicals. The pD2 in the SOD + xanthine/xanthine oxidase-treated vessels rings (7.19 +/- 0.11) was significantly lower than control vessel rings (7.49 +/- 0.04) and significantly higher than xanthine/xanthine oxidase-treated vessels (6.89 +/- 0.06). Catalase (1000 U/ml) also partially attenuated the loss of vascular norepinephrine responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of reactive oxygen metabolites on norepinephrine-induced vasoconstriction. 807 Jun 89


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