Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the direct method of pulse radiolysis to determine the superoxide dismutase like activity of copper(II) cimetidine complexes, it was found that the reaction rate constant with O2-, kcat, was (8.5 +/- 0.5) x 10(8) M-1s-1 independent of the cimetidine concentrations present in excess of 50-200 microM over the metal. The results suggest that either the 1:1 ligand to metal complex does not catalyze O2- dismutation at a comparable rate to that of the 2:1 complex, or that the stability constant of the last species is much higher than that determined earlier by Kimura et al., and only the 2:1 species is present in the solutions. With the indirect methods of cytochrome c and NBT for determining the ability of these complexes to catalyze O2 dismutation, these compounds exhibited a much lower SOD activity, and kcat was determined to be (5.0 +/- 0.3) x 10(6) and (7.6 +/- 0.4) x 10(7) M-1s-1, respectively using the two assays.
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PMID:Determination of the superoxide dismutase-like activity of cimetidine-Cu(II) complexes. 164 90

We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.
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PMID:Effect of superoxide dismutase in cats with cold-induced edema. 216 63

We evaluated the effect of SOD, an oxygen-free radical scavenger, on peritumoral edema in 20 rabbits. The VX2 carcinoma was transplanted to the brains of these New Zealand white rabbits. Detection of superoxide radicals in vitro was performed by incubating the VX2 tumor cells with NBT. For evaluation of the effect of SOD on the tumor cells, they were treated with free SOD or PEG-SOD before and after incubation with NBT. The animals were separated into three groups: group 1, control group; group 2, SOD-untreated tumor group; group 3, two SOD-treated groups-group 3a, treated with 10,000 U/kg PEG-SOD on day 1 and 4 after tumor transplantation and sacrificed on day 13; group 3b, treated with 10,000 U/kg PEG-SOD on day 7 and 10 and sacrificed on day 13. Brain edema was assessed by SG measurement. Our preliminary in vitro data indicated that the VX2 carcinoma produced superoxide radicals but that free SOD and PEG-SOD could not penetrate into tumor cells nor inhibit superoxide radicals. In vivo data also indicated that PEG-SOD failed to reduce peritumoral edema. It was concluded that intracellular uptake or penetration of SOD must first be achieved before any effect on peritumoral edema can be assessed.
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PMID:Effect of superoxide dismutase in rabbits with peritumoral edema. 216 69

The effect of recombinant human superoxide dismutase (rh-SOD) on infarct size was investigated in porcine hearts. The left anterior descending coronary artery was occluded in each of 24 anesthetized pigs for 45 min and reperfused for 24 h. The animals were randomly assigned to either rh-SOD (n = 12) or placebo treatment (n = 12). 2 min before reperfusion, an intracoronary (i.c.) infusion of rh-SOD (total dose: 2000 U/kg) or placebo was started which lasted for up to 45 min reperfusion. At the end of the experiment, the infarcted myocardium was assessed using a tetrazolium stain (NBT) and related to the risk region which was determined with a fluorescent dye. Two pigs of the SOD group and one of the control group died before the end of the experiments. Except for a lower calculated myocardial oxygen consumption and a lower dp/dtmax in the SOD group during ischemia, hemodynamic parameters of the two groups did not differ significantly. rh-SOD i.c. treatment during reperfusion did not reduce infarct size significantly. Infarct size amounted to 74 +/- 13% in the control group and to 66 +/- 19% in the treated group. The incidence of reperfusion arrhythmias was not affected by rh-SOD treatment. It is concluded that i.c. rh-SOD treatment at the beginning of reperfusion neither significantly reduces infarct size nor diminishes the incidence of reperfusion arrhythmias in this preparation.
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PMID:Intracoronary superoxide dismutase for the treatment of "reperfusion injury", A blind randomized placebo-controlled trial in ischemic, reperfused porcine hearts. 329 62

The capacity of macrophages activated in vivo and in vitro to kill Plasmodium yoelii was investigated. Macrophages activated by BCG-, Con A-, or malaria-induced lymphokines (LK) were cultured with P. yoelii-parasitized erythrocytes (PE). In some experiments, effector and target cells were separated by a 0.45-micron filter. Parasite viability was assessed a) in vivo by injection of mice and quantitative detection of parasites by RIA or b) in vitro by the incorporation of 3H amino acids into parasite proteins. Activated macrophages killed target PE in a dose-dependent manner by elaborating a membrane-permeable soluble factor(s). The addition of small amounts of immune serum augmented the killing of the parasites. LK-activated macrophages underwent an oxidative burst upon the phagocytosis of PE as evidenced by the accumulation of reduced formazan in the NBT assay. The magnitude of the oxidative response corresponded to the number of parasites that were ingested. The phagocytosis-induced oxidative burst was necessary for subsequent killing of Plasmodium. Parasites incubated in microchambers separated from macrophages by a 0.45-micron filter were susceptible to H2O2 released by LK-activated macrophages incubated with PMA, opsonized zymosan, or P. yoelii antigen. Inhibition of protein synthesis by parasites exposed to products of activated macrophages was abrogated by preincubating macrophages with catalase but not with SOD, mannitol, or histidine. These results suggest that phagocytosis-associated oxidative mechanisms mediate the destruction of the malaria parasite. Hence, cell-mediated as well as antibody-dependent mechanisms cooperate in the immune response against malaria.
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PMID:Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages. 669 Jun 6

Different physicochemical studies were undertaken with polycrystalline samples of the complex [Cu2(carnosine)2(H2O)2].2H2O. The infrared spectrum was discussed in comparison with that of free carnosine and on the basis of the known structural data. Magnetic susceptibility measurements were performed between 4.2 and 300 K, showing an effective magnetic moment of 1.79 BM. Both the electronic (reflectance) and ESR spectra were compatible with the existence of a dx2-y2 ground state. The axial reversed ESR spectrum could be explained on the basis of a very weak interdimeric coupling mechanism. The electrochemical behavior, investigated by cyclic voltammetry, shows that the complex possesses a very high redox stability. The possible SOD-like activity was tested using the NBT/superoxide reduction assay. The results show a negligible SOD activity.
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PMID:Spectroscopic, magnetic, and electrochemical behavior of the copper(II) complex of carnosine. 750 89

NADPH diaphorase activity was found in membrane of DMSO-induced differentiated human promyelocytic leukemia HL-60 cells. This membrane-bound diaphorase activity increased dramatically during differentiation of HL-60 cells. A dye reductase was extracted from membrane of DMSO-induced differentiated HL-60 cells with n-octyl glucoside and sodium cholate in the presence of several protease inhibitors such as PMSF, DIFP, TLCK, antipain, chymostatin, leupeptin, pepstatin A and trypsin inhibitor. The NADPH diaphorase was highly purified by two-stage sequential column chromatographies. The purified enzyme, showing both SOD-insensitive cytochrome c and NBT reductase activities, migrated with an apparent molecular mass of 77 kDa on SDS-PAGE. When the purification of this diaphorase was carried out in the presence of only three protease inhibitors, PMSF, DIFP and TLCK, a partially proteolyzed form of the diaphorase with a molecular mass of 68 kDa was prepared. The proteolyzed diaphorase exhibited only an NADPH-dependent cytochrome c reductase. The NADPH diaphorase gave a positive cross-reaction to polyclonal antibodies raised against microsomal NADPH-cytochrome P450 reductase from rabbit liver.
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PMID:Purification of an NADPH-dependent diaphorase from membrane of DMSO-induced differentiated human promyelocytic leukemia HL-60 cells. 769 24

Tumor cells (AH130 hepatoma cell originated from rat) were injected intraportally into Donryu rats to produce liver metastases 21 days later. Phagocyte cells activity was depressed by the administration of Silica, which significantly increased the number of surface liver metastases. Phagocyte cells were stimulated by beta 1-3-glucan, which significantly reduced the number of metastases. And the administration of free radical scavenger (SOD, Catalase) increased the number of metastases. Non parenchymal cells (NPC) of the liver play a main role of self defence line for portally liver metastases. Then free radical from these cells were noticed in this study. NPC were isolated, from pronase perfused rat liver. O2- production by activated NPC was measured by chemiluminescence with CLA. NPC activated by beta 1-3-glucan added sera increased the luminescence of CLA, and SOD depressed the production of chemiluminescence. SOD activity of hepatocytes and tumor cells (AH130) were measured by NBT methods. Hepatocytes had high potential production of SOD, in contrast AH130 had poor production. These results suggest that free radicals from liver NPC was important for protecting liver metastases.
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PMID:[The effect of free radicals from non-parenchymal cells (NPC) of the liver on the development of liver metastases in rat]. 823 83

The influence of low level laser (LLL) irradiation at wavelength at 660 and 904 nm on oxidative stress (lipid peroxidation activity-LP, production of superoxide anion radicals-NBT reduction), activity of enzymes of antioxidative defense (superoxide dismutase-SOD, glutathione reductase-GR) and functional activity of sodium pump (Na+K+ ATPase) in relation with applied wavelength of LLL was investigated. The investigation was performed at the adult rabbits (n = 21) classificated in three groups: control group (C), the group of rabbits irradiated with LLL wavelength 904 nm (CL1) and the group of rabbits irradiated with LLL wavelength 660 nm (CL2). The irradiation was performed in the upper cervical region in the anatomical projection of the brainstem. It was established that LLL induced oxidative stress in the brainstem and the cortex of treated rabbits, independently of applied wavelength of laser beams. The registrated changes in functional activity of sodium pump were dependent on the applied wavelength. The irradiation at 904 nm caused the significant increase of the substrate uptake rate of sodium pump in the brainstem tissue. The irradiation at 660 nm caused the "competitive inhibition" of the sodium pump. Decrease of norepinefrine content in the brainstem of treated rabbits pointed on the indirect mechanism of functional activity of sodium pump as well as the oxidative stress.
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PMID:Influence of low level laser irradiation on biochemical processes in brainstem and cortex of intact rabbits. 948 29

The tetrapeptide-Cu(II) complex H-(l-His-Gly)2-OH/Cu(II), indicated as L-Cu(II), has been investigated, as compared to the Cu(II) inorganic salt CuSO4, for its antioxidative and anti-inflammatory properties under a panel of experimental conditions. Both inorganic and organic Cu(II) compounds showed comparable activities in vitro and ex vivo by: (i) protecting, in a dose-dependent manner, rat brain homogenates from Fe(III)/ascorbate- or haemoglobin-induced lipid peroxidation; (ii) inhibiting the superoxide-mediated ferricytochrome c reduction by activated macrophages. CuSO4 and L-Cu(II) also exhibited similar anti-inflammatory effects in vivo by reducing significantly the extent of carrageenan-induced edema in the rat paw. The activities of the two compounds diverged strikingly only in the xanthine/xanthine oxidase system at low phosphate buffer concentration. L-Cu(II) decreased the rate of NBT reduction by superoxide in a true SOD-like fashion without affecting urate production. Instead, Cu(II) ions caused the rapid xanthine oxidase inactivation thus inhibiting both urate and superoxide production; this effect might be ascribed to the superoxide-mediated generation of the strong oxidant Cu(III) and its interaction with the enzyme. The administration of Cu(II), whether complexed with linear oligopeptides or as an inorganic salt, to animals or tissue extracts, conferred protection against oxidation and ought, conceivably, to interact with endogenous biological molecules and form highly bioavailable complexes which serve, subsequently, as the real scavengers. Moreover, the claimed prominent scavenger activities of Cu(II)-oligopeptide complexes over inorganic copper ions could be realised only in very simple in vitro systems through mechanisms which, although of biochemical interest, are unlikely to be of physiopathological significance.
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PMID:An in vivo, ex vivo and in vitro comparative study of activity of copper oligopeptide complexes vs Cu(II) ions. 977 91


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