Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen free radicals (OFRs) have been implicated in the pathogenesis of an increasing number of diseases and inflammatory states. They may cause cell and tissue damage by their chemical modification of proteins, carbohydrates, nucleotides, and lipids. Under physiological conditions OFRs are part of normal regulatory circuits and are neutralized by antioxidants. Infections are one cause of increased OFR production. The aims of our study were to assess whether the increased oxidative stress in experimental otitis media with effusion (OME) is reflected in erythrocytes by lipid peroxidation and to survey the alterations in oxidant and antioxidant enzyme activities in experimental OME in guinea pigs. Erythrocyte total (enzymatic plus non-enzymatic) superoxide scavenger activity (TSSA), non-enzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD), catalase (CAT), and xanthine oxidase (XO) activities, and malondialdehyde (MDA) level were measured in 6 guinea pigs with OME and in 6 controls. The TSSA, SOD, XO activities, and MDA level in experimental OME were significantly higher than in controls. No significant differences were found in erythrocyte NSSA and CAT activities. In experimental OME induced by histamine injection, increased OFR production was observed, suggesting that OFRs may play an important role in cell and tissue damage due to OME.
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PMID:Evaluation of oxidative stress in erythrocytes of guinea pigs with experimental otitis media and effusion. 1281 29

Infections with the microaerophilic protozoan parasite Trichomonas vaginalis are commonly treated with metronidazole, a 5-nitroimidazole drug. Metronidazole is selectively toxic to microaerophiles and anaerobes because reduction at the drug's nitro group, which is a precondition for toxicity, occurs only quantitatively in these organisms. In our previous work we identified the flavin enzyme thioredoxin reductase as an electron donor to 5-nitroimidazole drugs in T. vaginalis and observed that highly metronidazole-resistant cell lines lack thioredoxin reductase and flavin reductase activities. In this study we added the flavin inhibitor diphenyleneiodonium (DPI) to T. vaginalis cultures in order to test our hypothesis that metronidazole reduction is catalyzed by flavin enzymes, e.g. thioredoxin reductase, and intracellular free flavins. Indeed, within hours, DPI rendered T. vaginalis insensitive to metronidazole concentrations as high as 1mM and prevented the formation of metronidazole adducts with proteins. Thioredoxin reductase activity was absent from DPI-treated cells and flavin reductase activity was sharply decreased. In addition, DPI-treated cells also upregulated the expression of antioxidant enzymes, i.e. thioredoxin peroxidases and superoxide dismutases, and displayed a fundamentally altered metabolism caused by inactivation of pyruvate:ferredoxin oxidoreductase (PFOR) and concomitant upregulation of lactate dehydrogenase (LDH) activity. Thus, the disruption of the cellular flavin metabolism by DPI mediated metabolic steps which are similar to that of cells with metronidazole resistance induced in vitro. Finally, we present direct evidence that the increased expression of antioxidant enzymes is dispensable for acquiring resistance to metronidazole.
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PMID:The flavin inhibitor diphenyleneiodonium renders Trichomonas vaginalis resistant to metronidazole, inhibits thioredoxin reductase and flavin reductase, and shuts off hydrogenosomal enzymatic pathways. 2009 43