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)

Trauma and anaesthetics are responsible for local and general change in the organism. The characteristic changes in metabolism are caused by hormones. In addition, the increased glycogenolysis, gluconeogenesis, proteolysis and lipolysis are characteristic of this catabolic metabolism. Three groups (injured patients, patients with pulmonary disease, multiple trauma patients) showed an elevated lipid peroxidation as indicated by increased formation of TBA-reactive substances in the post-trauma or after surgery phase. The production of free radicals is supported by several stress factors. In this connection, the state of metabolism of the patients, several anaesthetics and the artificial respiration is very important. Enzymatic protecting systems (SOD, GSH-Px, Catalase) react to oxidative stress by positive adaptation. The non-enzymatic antioxidative systems (tocopherol, ascorbic acid, selen) are diminished, indicating an increased requirement.
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PMID:[Antioxidant status after surgical stress]. 228 19

I examined the effects of host cells reactive to foreign bodies such as plastic plate or hemostatic spongel on the progression of tumor cells. QR tumor cells spontaneously regressed in normal C57BL/6 mice apparently associated with a reduction in production of PGE2 by the tumor cells. I have observed that such regressor tumor cells are able to grow lethally when implanted in mice after having been attached to plastic plate. The clones which were derived from these plastic plate-derived tumors in normal mice maintained their growth potential when they were injected into other normal mice. Furthermore the arising tumors produce much higher levels of PGE2 than the original QR tumor cells. Interestingly, I could not observe acquisition of tumorigenicity or a higher level of PGE2-production in the clones obtained from the arising tumors which were grown in 10Gy-irradiated mice. Moreover, QR tumor cells are able to grow in mice when they are injected at the site where plastic plate had been implanted about 30 days previously. These results indicate that the restoration of tumorigenicity of QR tumor cells is not only due to attachment to plastic plate, but also mediated by radiation-sensitive host cells reactive to plastic plate which enhance the progression of tumor cells. Similar results are also obtained by coinoculation of QR tumor cells with host reactive cells which had been induced by implantation of hemostatic spongels into the peritoneal cavity of mice. Greater amounts of PGE2-production by QR tumor cells were observed when the tumor cells were cocultured with spongel reactive cells. This PGE2-production was markedly inhibited by the presence of radical scavengers (Catalase, Mannitol, SOD + Catalase) in the coculture medium(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Progression of regressor tumor cells by host reactive cells to such foreign bodies as plastic plate and hemostatic spongel]. 237 14

Adherent human mesangial cells (HMC) were unable to phagocytose serum-treated zymosan (STZ), nevertheless this stimulus (1 mg/ml) induced a marked immediate increase of H2O2 and O2- release at a rate of 3.15 +/- 0.35 and 3.40 +/- 0.12 nmol/10(6) HMC/hr, respectively. Zymosan alone resulted in no release of either H2O2 or O2-. Phorbol myristate acetate (PMA, 2 X 10(-6) M) had only marginal effects on HMC leading to the generation of 0.273 +/- 0.014 nmol O2-/10(6) HMC/hr. After a lag period, human recombinant tumor necrosis factor-alpha (TNF-alpha) and human recombinant interleukin 1-alpha IL-1 alpha) both induced significant O2- production measured as SOD inhibitable reduction of cytochrome c, 5 X 10(-5) M, by adherent HMC for up to five hours, the maximum rates being 3.04 +/- 0.08 and 3.2 +/- 0.08 nmol/10(6) HMC/hr for IL-1 alpha and TNF-alpha, respectively. Significant O2- release was detectable at 0.625 ng/ml (37 pM) IL-1 alpha or 1 ng/ml (59 pM) TNF-alpha (P less than 0.05). Catalase inhibitable H2O2 production was also induced by IL-1 alpha and TNF-alpha in a dose dependent manner. Using scopoletin (40 nM) and 1 microM peroxidase we fluorimetrically measured 1.73 +/- 0.14 and 1.49 +/- 0.19 nmol H2O2/10(6) HMC/hr induced by IL-1 alpha (25 ng/ml) and TNF-alpha (20 ng/ml). Finally, we ascertained the type of radical species produced by HMC stimulated by cytokines employing ESR-spin-trapping with DMPO.2+ These results demonstrated that O2- was the primary radical species formed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin 1-alpha and tumor necrosis factor-alpha induce oxygen radical production in mesangial cells. 240 88

1. Superoxide dismutase (SOD, 60 u ml-1) or ferricytochrome c (70 microM) significantly inhibited thrombin-stimulated platelet adhesion to gelatin-coated plastic, whereas catalase (1000 u ml-1) or mannitol (1 mM) had no effect. 2. The platelet aggregation induced by low concentrations of thrombin (causing less than 45% maximal change in light transmission) was inhibited by SOD. Catalase or mannitol had no effect on platelet aggregation. 3. Pyrogallol (an O2- generator) enhanced both platelet adhesion to gelatin-coated plastic and platelet aggregation induced by thrombin; this enhancement was neutralized by SOD. 4. These results indicate that O2- increase both platelet adhesion and aggregation, whereas other free radicals such as hydrogen peroxide or hydroxyl radicals are not involved.
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PMID:Superoxide anions enhance platelet adhesion and aggregation. 255 40

The effects of hypoxanthine (HX) and xanthine oxidase (XO) on the (3H)-dopamine (DA) uptake into synaptosomes of rat striatum were examined. Preincubation with 20 mU XO and 0.25 mM HX for 10 min diminished the uptake to 55% of controls. Under these conditions no increase of TBARS as an indicator of lipid peroxidation was observed. Kinetic studies revealed that the decrease in DA uptake was related to the high-affinity transport whereas the low-affinity transport carrier remained unaffected. SOD did not influence uptake inhibition, Catalase completely restituted DA uptake at an activity of 50 U. Thus, hydrogen peroxide and the hydroxyl radical appears to be involved in the deleterious action of HX/XO. The effects of this radical generating system seems to be directed to specific sites of biological membranes.
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PMID:Influence of the hypoxanthine/xanthine oxidase system on striatal (3H) dopamine uptake. 273 Jun 11

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

It has already shown that catalase activity is significantly decreased in red cells of patients with P. falciparum. The mechanism suggested was by this enzyme inactivation through increased H2O2 generated during malarial infection. The present study was performed to verify this hypothesis. Catalase activities of red cells with high or low parasitemia in patients with P. falciparum were found to be lower than those of normal red cells. However, P. falciparum-infected red cells cultured for one week showed similar SOD and catalase levels to normal red cells. There was also no significant difference in the catalase levels between the parasitized and non-parasitized red cells. The difference in catalase activity of infected red cells before and after culture could be explained in terms of the activation of mononuclear cells and macrophages in vivo. During the sojourn of the parasitized red cells in close proximity to the macrophages of the spleen, they might trigger oxidative bursts resulting in increased H2O2. In order to protect themselves from oxidant damage, the catalase in the infected red cells could be inactivated by H2O2 resulting in the reduction of this enzyme.
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PMID:Superoxide dismutase and catalase activities of cultured erythrocytes infected with Plasmodium falciparum. 307 Jul 68

The metabolic disorder, alkaptonuria, is distinguished by elevated serum levels of 2,5-dihydroxyphenylacetic acid (homogentisic acid), pigmentation of cartilage and connective tissue and, ultimately, the development of inflammatory arthritis. Oxygen radical generation during homogentisic acid autoxidation was characterized in vitro to assess the likelihood that oxygen radicals act as molecular agents of alkaptonuric arthritis in vivo. For homogentisic acid autoxidized at physiological pH and above, yielding superoxide (O2-)2 and hydrogen peroxide (H2O2), the homogentisic acid autoxidation rate was oxygen dependent, proportional to homogentisic acid concentration, temperature dependent and pH dependent. Formation of the oxidized product, benzoquinoneacetic acid was inhibited by the reducing agents, NADH, reduced glutathione, and ascorbic acid and accelerated by SOD and manganese-pyrophosphate. Manganese stimulated autoxidation was suppressed by diethylenetriaminepentaacetic acid (DTPA). Homogentisic acid autoxidation stimulated a rapid cooxidation of ascorbic acid at pH 7.45. Hydrogen peroxide was among the products of cooxidation. The combination of homogentisic acid and Fe3+-EDTA stimulated hydroxyl radical (OH.) formation estimated by salicylate hydroxylation. Ferric iron was required for the reaction and Fe3+-EDTA was a better catalyst than either free Fe3+ or Fe3+-DTPA. SOD accelerated OH. production by homogentisic acid as did H2O2, and catalase reversed much of the stimulation by SOD. Catalase alone, and the hydroxyl radical scavengers, thiourea and sodium formate, suppressed salicylate hydroxylation. Homogentisic acid and Fe3+-EDTA also stimulated the degradation of hyaluronic acid, the chief viscous element of synovial fluid. Hyaluronic acid depolymerization was time dependent and proportional to the homogentisic acid concentration up to 100 microM. The level of degradation observed was comparable to that obtained with ascorbic acid at equivalent concentrations. The hydroxyl radical was an active intermediate in depolymerization. Thus, catalase and the hydroxyl radical scavengers, thiourea and dimethyl sulfoxide, almost completely suppressed the depolymerization reaction. The ability of homogentisic acid to generate O2-, H2O2 and OH. through autoxidation and the degradation of hyaluronic acid by homogentisic acid-mediated by OH. production suggests that oxygen radicals play a significant role in the etiology of alkaptonuric arthritis.
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PMID:Homogentisic acid autoxidation and oxygen radical generation: implications for the etiology of alkaptonuric arthritis. 312 48

Xanthine oxidase with acetaldehyde as substrate (the XOA system) generated superoxide anion and hydrogen peroxide, but this system had only weak bactericidal activity. Addition of Fe2+ and EDTA to the XOA system (XOA-Fe-EDTA system) increased bactericidal activity against Staphylococcus aureus, Escherichia coli, Listeria monocytogenes and Salmonella typhimurium, although both Mycobacterium tuberculosis and Candida albicans remained highly resistant. Catalase (H2O2 scavenger) and mannitol (.OH scavenger) almost completely inhibited the bactericidal activity of the XOA-Fe-EDTA system whereas SOD (O2- scavenger) was less inhibitory. Azide (1O2 scavenger) caused no such inhibition. The results suggest the possible role of .OH, H2O2 and O2- in the XOA-Fe-EDTA-mediated antimicrobial system, as effector molecules. There was no correlation between resistance of a given bacterium to active oxygen and the level of endogenous active oxygen-scavengers.
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PMID:Susceptibility of micro-organisms to active oxygen species: sensitivity to the xanthine-oxidase-mediated antimicrobial system. 312 35

Methods have been developed for the measurements of catalase and superoxide dismutase (SOD) in single, isolated muscle fibers. These fibers are also classified according to fiber type. Catalase is determined using a fluorescent method for the measurement of hydrogen peroxide consumed. SOD measurements are carried out using a modification of established techniques whereby the inhibition of oxidation of epinephrine by SOD is assayed fluorometrically. Both enzymes may be determined in submicrogram samples of dried muscle. This approach avoids the complication of the inclusion of nonmuscle tissue with varying enzymatic activities which is frequently experienced when using homogenates of muscle, particularly diseased muscle. In addition, these techniques can be used to determine the inherent variation in SOD and catalase activities within individual fibers of the same fiber type. The Km and Vmax for catalase, determined using homogenates of human muscle, were found to be 12 mM and 1.45 mumol/min/mg dry wt, respectively. Catalase of muscle was inhibited 50% by 2 microM sodium azide. Mn-SOD contributes less than one-fifth of the total SOD activity. Therefore the activity is largely due to the Cu-Zn form of SOD. These methods are applicable to a wide variety of tissues.
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PMID:Micromethods in single muscle fibers. 1. Determination of catalase and superoxide dismutase. 323 59


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