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)

Myeloperoxidase is virucidal to human immunodeficiency virus type 1 (HIV-1) in the persistently infected CEM human T-cell line or in acutely infected human peripheral blood mononuclear cells, as judged by viral infectivity and P24 radioimmunoassay. HIV-1 was specifically inactivated by low doses of the human myeloperoxidase (1.4 to 14.3 mU/ml) and the cells were spared. A higher enzyme concentration (143 mU/m) was cytotoxic, but uninfected CEM cells and normal lymphocytes were resistant to > or = 143 mU of myeloperoxidase per ml. The enzyme was virucidal with the Cl- present in medium and did not require exogenous H2O2. Catalase, an antioxidant enzyme, partially inhibited the virucidal effect of myeloperoxidase. Hence, the H2O2 probably came from the HIV-infected cells themselves. These in vitro findings indicate that the myeloperoxidase system is capable of inactivating HIV-1 of infected cells.
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PMID:Virucidal effect of myeloperoxidase on human immunodeficiency virus type 1-infected T cells. 806 78

The long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) contains sequences required for the initiation of gene transcription. Among the substances known to activate the HIV-1 LTR is hydrogen peroxide (H2O2). We report here that H2O2-induced activation of the LTR in the macrophage cell line THP-1 and the lymphocyte cell line, Jurkat, is greatly increased by vanadate. Activation of the LTR by phorbol myristate acetate, tumor necrosis factor alpha, lipopolysaccharide, or Staphylococcus epidermidis extract was not increased by vanadate, indicating some selectivity for H2O2. H2O2 and vanadate also acted synergistically to increase the production of HIV-1 virions by the latently infected macrophage cell line U-1 as determined by p24 antigen release and the detection of intact virions by electron microscopy. Effects were observed at H2O2 and vanadate concentrations down to 3 x 10(-6) M, with high concentrations leading to cell toxicity. Catalase was strongly inhibitory when added prior to the interaction of H2O2 and vanadate, but was considerably less inhibitory when the H2O2 and vanadate were allowed to preincubate prior to the catalase addition. H2O2 reacts with vanadate to form peroxides of vanadate that have potent biological effects. Our findings suggest that among these is the activation of the HIV-1 LTR.
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PMID:Activation of the HIV long terminal repeat and viral production by H2O2-vanadate. 872 29

A homeostatic balance exists between the cellular generation of oxidant species and endogenous antioxidants under normal physiological conditions. Human Immunodeficiency Virus (HIV) infection is known to affect this balance causing oxidative stress. However, the interaction of HIV infection with a substance abuse on cellular oxidant/antioxidant system is sparse. This study was designed in order to investigate the interactive effect of morphine abuse and Simian Immunodeficiency Virus/ Simian Human Immunodeficiency Virus (SIV/SHIV) infection on plasma oxidant/antioxidant balance in rhesus macaques. Six rhesus macaques adapted to morphine dependence (20 weeks) along with three controls were infected with mixture of SHIV(KU-1B), SHIV(89.6P), and SIV(17E-Fr). Plasma samples from morphine-dependent and control macaques were analyzed for an array of oxidative stress indices after 16 weeks of infection. Morphine-dependence significantly increased plasma malondialdehyde (MDA) and 8-isoprostane levels (8-fold and 2-fold), but these animals showed higher MDA and 8-isoprostane levels after viral infection (18-fold and 4-fold) which was directly correlated with increase in viral load and decline in CD4+ cells. Plasma glutathione (GSH) level depleted (55%) with morphine dependence that was further depleted (25%) by the infection. Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were increased by 30% and 110%, respectively with morphine dependence, but that was decreased by the infection. Catalase (CAT) activity declined (25%) with morphine dependence that was further declined by infection. Our results clearly suggest that morphine interaction with SIV/SHIV infection causes higher oxidative tissue injury that might have implication in the pathogenesis of AIDS in morphine-dependent macaques.
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PMID:Interaction of SIV/SHIV infection and morphine on plasma oxidant/antioxidant balance in macaque. 1793

Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by defects of nicotinamide adenine dinucleotide phosphate oxidase. Catalase-positive bacteria and fungi are phagocytosed, but persist within phagocytes, resulting in granulomatous inflammation. Although allogeneic hematopoietic stem cell transplantation (HSCT) is a curative treatment for CGD, HSCT sometimes leads to fatal outcomes related to the exacerbation of persistent infectious or post-infectious inflammatory diseases, particularly in adolescent and young adult patients with a history of recurrent infections and/or multiple granulomas in organs. Here, we present the case of a young adult with X-linked CGD in whom multiple lesions were found in lungs and lymph nodes on both computed tomography and positron emission tomography (PET) scans before allogeneic HSCT, but all the lesions disappeared only on PET scan 5 months after HSCT. Monitoring the activity of multiple pre-existing lesions with PET scan may be beneficial to adolescent and young adult CGD-patients undergoing allogeneic HSCT.
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PMID:Dramatic Improvement in the Multifocal Positron Emission Tomography Findings of a Young Adult with Chronic Granulomatous Disease Following Allogeneic Hematopoietic Stem Cell Transplantation. 2536 70