Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.15.1.1 (superoxide dismutase)
58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Linkage studies were performed in three families (A, B, and C) with autosomal dominantly inherited parkinsonism affecting multiple members in three generations. Affected individuals exhibited the cardinal signs and symptoms of Parkinson's disease, with a mean age of onset of 51, 62, and 61 years in Families A, B, and C, respectively. Parkinsonian symptoms responded to L-dopa treatment, and an [18F]6-fluoro-L-dopa positron emission tomography scan in 1 affected member of Family B showed decreased striatal uptake typical of Parkinson's disease. Ancestors of all three families were traced to a small region in northern Germany and southern Denmark, suggesting the possibility of a common mutation. Linkage studies were performed with polymorphic markers associated with the following candidate genes: the genes for glutathione peroxidase (GPX1, 3q11), tyrosine hydroxylase (TH, 11p15.5), brain-derived neurotrophic factor (BDNF, 11p14), catalase (CAT, 11p13), amyloid precursor protein (APP, 21q21), copper-zinc superoxide dismutase (SOD1, 21q21), and debrisoquin 4-hydroxylase (CYP2D6, 22q13.1). Summed lod scores for all families excluded linkage to the genes GPX1, TH, APP, SOD1, and CYP2D6, as well as to the chromosomal region containing the genes CAT and BDNF. If families were analyzed individually, exclusion was possible for two (Family A), six (Family B), and five (Family C) of the seven candidate genes. There was strong evidence against linkage for the remaining loci in all families analyzed individually, except for TH, which was uninformative in Families A and B, and CYP2D6, which gave slightly positive pairwise lod scores in Family A. Our results indicate that the candidate genes investigated are not involved in the etiology of parkinsonism in these families.
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PMID:Genetic linkage studies in autosomal dominant parkinsonism: evaluation of seven candidate genes. 791 97

Free radical modes of cytotoxicity of streptonigrin (STN) and Adriamycin (ADR) in Chinese hamster V79 cells under aerobic conditions were evaluated using 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TP), a low molecular weight stable nitroxide free radical with antioxidant properties and desferrioxamine (DF), a transition metal chelator. In addition, exogenous superoxide dismutase (SOD, EC 1.15.1.1) and catalase (CAT, EC 1.11.1.6), were tested for cytoprotective effects. EPR studies showed that TP reacts with the semiquinones of both ADR and STN and also with O2- radicals generated during aerobic redox cycling of the respective semiquinone radicals. Pulsed field gel electrophoresis studies confirmed that DNA double-strand breaks (dsb) induced by STN in V79 cells were inhibited completely by TP, whereas ADR-induced DNA dsb were not affected by TP. Clonogenic cell survival studies showed that STN-induced cytotoxicity could be inhibited completely by DF or TP. Both agents were ineffective in inhibiting ADR-induced cytotoxicity. SOD and CAT were ineffective in protecting against both STN and ADR cytotoxicity. Our results are consistent with a mechanism requiring the semiquinone radical intermediate of STN for cytotoxicity and minimal free radical involvement in ADR-induced V79 cell cytotoxicity.
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PMID:Free radical modes of cytotoxicity of adriamycin and streptonigrin. 794 43

The aim of the present investigation was to evaluate the putative involvement of oxygen free radicals in interleukin-1 beta (IL-1 beta)-induced suppression of islet glucose oxidation. Isolated adult rat pancreatic islets were exposed for 1 h to liposomally encapsulated superoxide dismutase (SOD; 10 mg/ml), catalase (CAT; 10 mg/ml) and glutathione peroxidase (GPX; 5 mg/ml), after which IL-1 beta (25 U/ml) or hydrogen peroxide (H2O2; 0.1 mM) was added, and the incubation was continued overnight. The following day, samples were taken from the incubation media for nitrite determinations, and islet glucose oxidation rates were measured. The CAT activity increased fourfold after addition of CAT-containing liposomes. It was found that IL-1 beta induced a marked increase in islet nitrite production, as an index of nitric oxide formation, and that this was paralleled by a decrease in islet glucose oxidation rates. H2O2-treated islets exhibited a modest decrease in glucose oxidation rates and a minor increase in the release of nitrite to the media. Treatment of islets with liposomes containing the antioxidant enzymes SOD, CAT and GPX, either alone or in combination, did not decrease the effect of IL-1 beta. However, the H2O2-induced decrease in glucose oxidation rates was counteracted by the combination of the antioxidants. It was concluded that, provided the intracellular delivery of the antioxidant enzymes to the islet cells was effective, oxygen free radicals probably do not play a decisive role in IL-1 beta suppression of islet glucose metabolism.
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PMID:Liposomal delivery of antioxidant enzymes protects against hydrogen peroxide- but not interleukin-1 beta-induced inhibition of glucose metabolism in rat pancreatic islets. 796 13

Menhaden fish oil (FO) containing n-3 fatty acids dramatically extends the life span and delays the onset and progression of autoimmune disease in (NZBxNZW)F1 (B/W) female mice as compared to those fed corn oil (CO) rich in n-6 lipids. As an inefficient antioxidant defense system has been linked to autoimmune diseases, the present study was undertaken to determine whether the protective action of n-3 lipids is mediated through their antioxidant defense system. Weanling B/W mice were fed a nutritionally adequate, semipurified diet containing CO or krill oil (KO) or FO at 10% level (w/w) ad libitum until the mice were 6.5 months old. All diets contained the same level of vitamin E (21.5 mg/100 g diet). We compared the effects of feeding n-6 and n-3 lipids on survival, kidney disease, hepatic microsomal lipid composition, peroxidation, and on the activity and mRNA expression of the antioxidant enzymes catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in 6.5-month-old B/W mice. The results showed that when compared to livers from CO-fed mice, livers from KO- and FO-fed mice showed: (i) significantly higher (P < 0.001) activities and expression of CAT, GSH-Px and SOD; (ii) significantly lower (P < 0.001) arachidonic acid (20:4n-6) and linoleic acid (18:2n-6) and higher (P < 0.001) eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) levels in hepatic microsomes; and (iii) significantly lower (P < 0.001) estimated peroxidation indices and thiobarbituric acid reactive substances generation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of n-3 and n-6 fatty acids on the activities and expression of hepatic antioxidant enzymes in autoimmune-prone NZBxNZW F1 mice. 799 Jun 63

Caerulein-induced acute pancreatitis in rats commonly complicated ARDS-like acute lung injury. Acute pancreatitis induced by caerulein in the circulating neutrophil-depleted rat by hydroxyrea or with the administration of SOD, CAT or Pentoxifylline, the wet lung weight, lung capillary endothelial permeability decrease significantly compared to the caerulein group (P < 0.05). There are no lung morphologic evidences of neutrophil sequestration, interstial edema, intralveolar hemorrhage that seen in caerulein infusion animals. But it has no effect against the development of acute pancreatitis. It suggested that neutrophil and neutrophil-derived oxygen radical are the important mediators of acute lung injury complicated by pancreatitis.
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PMID:[The role of pentoxifylline in acute lung injury complicated by pancreatitis]. 799 67

The successful prevention of oxidative damage in E. coli B cells by cationized catalase (cCAT), and the induction of oxidative stress by cationized glucose oxidase (cGO) and cationized superoxide dismutase (cSOD) is presented in this study. Exposure of E. coli cells to hydrogen peroxide and hydroxyl radical resulted in a rapid killing of the cells. Measurements of biochemical markers: cellular potassium levels and uptake and accumulation of leucin indicated membrane damage in some of the oxidants employed. Following incubation with native CAT or SOD, the cells were washed and exposed to oxidative stress. The results of this procedure did not protect the cells against the oxidative damage. In contrast, incubation of the cells with pretreated CAT with poly-L-histidine, followed by washing of the cells and the subsequent introduction of oxidative stress inducers, resulted in a pronounced protection of the cells against the oxidative stress. Employment of pretreated SOD, and exposure, after washing the cells, to oxidative stress, resulted in an enhancement of the oxidative damage in some cases. Exposure of the cells to cGO resulted in a marked killing of the cells as compared to the untreated enzyme. The use of E. coli cells as a model system for studying the effect of cationized enzymes on cell surfaces is discussed.
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PMID:Prevention and induction of oxidative damage in E. coli cells by cationized proteins. 802

EDTA-chelated ferrous chloride (Fe(2+)-EDTA) mixed with ascorbic acid (VC) was shown in vitro to produce 2,3-dihydroxybenzoic acid (2,3-DHBA), one of the hydroxyl radical (.OH) derivatives formed from reaction with 1 mM salicylic acid. The .OH generating system of Fe(2+)-EDTA (5, 25 and 50 microM) mixed with VC (50, 250 and 500 microM) was perfused for 15 min to the isolated rat hearts to characterize the effect of exogenous .OH on cardiac function, metabolism, and structure. A dose-effect relationship was observed between .OH dosage and ventricular dysfunction, increase in coronary flow, structural damage, decrease in ATP and increase in lipid peroxidation. Catalase (CAT, 500 U/ml) and deferoxamine (DFX, 10 mM) significantly (P < 0.05) reduced .OH formation in vitro, but superoxide dismutase (SOD, 100 U/ml) did not. When these agents were given to the heart perfused with 50 microM Fe(2+)-EDTA plus 500 microM VC, SOD failed to modify any myocardial alterations whereas CAT and DFX completely reversed them. Addition of 500 microM hydrogen peroxide (H2O2) to the 50 microM Fe(2+)-EDTA plus 500 microM VC further caused a 14-fold increase in .OH generation. Addition of H2O2 (500 microM) to the .OH generating mixture induced more conspicuous myocardial changes compared with the mixture without H2O2 addition, but the extent of those changes other than increase in coronary flow was less than that caused by perfusion with 500 microM H2O2 alone. These results further suggest that the cardiac changes induced by the .OH generating system are due to the combined effects of .OH and H2O2 which is formed as an intermediate product.
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PMID:Characterization of exogenous hydroxyl radical effects on myocardial function, metabolism and ultrastructure. 807 2

An experiment was conducted on rats to investigate the capacity of antioxidants to protect against acute toxicity caused by DON or T-2 toxin. Male rats were fed two different feeds. One group received a feed deficient in vitamins C and E and selenium, whereas the other group was fed with a feed enriched in antioxidants. After two weeks, selected groups of rats were administered orally a single dose of DON or T-2 toxin. After the treatment with mycotoxins, all rats were decapitated. The livers were analyzed for TBARS values, hepatic GSH content and for the activities of CyP-450, CAT, SOD and GSH-TR. Increases in lipid peroxides of 21% and 268% were observed in those rats which did not receive the supplement of antioxidants and which were administered DON or T-2 toxin, respectively. There was no significant increases in the TBARS values in the groups receiving DON with selenium and vitamins, but increases of 57% and 79% were recorded in the groups administered T-2 toxin and antioxidants. Furthermore, in the groups fed the deficient feed and administered DON or T-2 toxin, the lipid peroxidation increased by 33% and 307%, respectively. No mortality, and a lower number of intoxicated animals were observed in rats fed a diet supplemented with antioxidants. Significant decreases of GSH, CAT, SOD, CyP-450 and GSH-TR were recorded in treated rats receiving the deficient feed. The results of this study demonstrate that trichothecenes stimulate lipid peroxidation with consequent decrease of GSH content, but that the dietary use of selenium, alpha-tocopherol and ascorbic acid provides protection against acute toxicosis caused by DON or T-2 toxin.
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PMID:Protective effect of antioxidants against free radical-mediated lipid peroxidation induced by DON or T-2 toxin. 809 93

In the present study we have assayed antioxidant enzymatic activities of SOD, CAT, GSH-Px, GSH-Red, and G6PD in erythrocytes from two children with hemolytic-uremic syndrome (HUS) during the acute phase of the disease and after their recovery; in addition, we have tested the percentage of hemolysis after 24-h incubation in PBS containing glucose (1 g/1000 mL) or in the presence of their own plasma. Endogenous plasmatic MDA levels were also evaluated as lipid peroxidation marker. A significant decrease in SOD activity was found in erythrocytes from HUS patients, and the addition of their own plasma further decreased SOD activity. Elevated percentage of hemolysis was found in HUS patients when RBCs were incubated in their own plasma; this last effect was less evident in PBS + glucose.
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PMID:Impaired antioxidant defense mechanisms in two children with hemolytic-uremic syndrome. 821 May 65

Cellular uptake of succinylated catalase (Suc-CAT; Mw 227 kDa), bovine serum albumin (Suc-BSA; Mw 70 kDa), superoxide dismutase (Suc-SOD; Mw 34 kDa) and soybean trypsin inhibitor (Suc-STI; Mw 21 kDa) was studied using primary cultures of bovine brain microvessel endothelial cells (BMECs) developed as an in vitro model of the blood-brain barrier. Large succinylated proteins (Suc-CAT, Suc-BSA) were taken up by BMECs whereas significant uptake was not observed for native proteins and small succinylated proteins (Suc-SOD, Suc-STI). Uptake of Suc-BSA was significantly inhibited at 4 degrees C and in the presence of endocytosis inhibitors. Large succinylated proteins, maleylated BSA and dextran sulfate also showed competitive inhibition against Suc-BSA uptake while small succinylated proteins and carboxymethyl dextran did not show any effect. These results indicate that microvessel endothelial cells obtained from the brain endocytose succinylated proteins via a scavenger receptor-mediated mechanism for polyanions, and in addition, the importance of molecular weight or total numbers of anionic charges per one molecule of proteins is suggested. Usefulness of direct succinylation of proteins for their delivery to the brain capillary endothelium is thus demonstrated.
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PMID:Specific uptake of succinylated proteins via a scavenger receptor-mediated mechanism in cultured brain microvessel endothelial cells. 821 90


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