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)

Recombinant interferon preparations caused a dose-dependent increase of human monocyte cytotoxicity to the K562 and Daudi cell lines. Both rIFN-gamma and rIFN-beta enhanced this function to a similar extent, while rIFN-alpha c had less effect when compared on the basis of their anti-viral effects. Endotoxin and concanavalin A increased basal monocyte cytotoxicity while phagocytosis of latex particles had no effect. The increased monocyte cytotoxic effect of rIFN-beta was completely abrogated by monoclonal antibody to IFN-beta, while monoclonal antibody to IFN-gamma had no effect. However, monoclonal antibody to IFN-gamma only reduced the increased cytotoxic effect caused by rIFN-gamma by 25%. Catalase inhibited both basal monocyte cytotoxicity and the increase in cytotoxicity following addition of rIFN-gamma only slightly, suggesting that mechanisms other than the oxidative burst were active and could be induced by rIFN-gamma.
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PMID:Enhancement of human monocyte cytotoxicity by both interferon-gamma and -beta and comparison to other stimuli. 251 81

Human neutrophils, incubated with phorbol myristate acetate (PMA), caused a rapid and substantial adenosine triphosphate (ATP) depletion in lymphoblastoid Daudi cells without producing lysis. Catalase (which destroys hydrogen peroxide), taurine and methionine (which scavenge hypochlorous acid), and chloride omission from the medium prevented the ATP fall. An ATP depletion comparable to that induced by neutrophils was observed by replacing neutrophils with an appropriate myeloperoxidase-H2O2-Cl- enzymatic system. Together, these data suggest that the neutrophil ATP depleting activity involves the myeloperoxidase-catalyzed transformation of H2O2 into HOCl. Moreover, the free H2O2 remaining in the neutrophil extracellular environment is ineffective. In fact, a comparable amount of enzymatically generated H2O2 did not cause Daudi cell ATP loss. A direct role for H2O2 in the neutrophil-induced Daudi cell ATP depletion was observed only under artificial conditions, that is, in the presence of the heme enzyme inhibitor azide, which prevented the HOCl production but dramatically augmented the extracellular H2O2 level. Similar levels of ATP depletion in Daudi cells were induced by amounts of reagent HOCl comparable to those generated by neutrophils. As the generated HOCl can rapidly react with a variety of neutrophil-derived nitrogenous compounds (primarily ammonia and taurine) to yield chloramines, these chlorinated oxidants might contribute to the neutrophil-mediated ATP depletion. Nevertheless, the main and well-characterized chloramines (ammonia-derived monochloramine, NH2Cl, and taurine monochloramine, TauNHCl) were devoid of ATP-depleting capacity. Thus, the results suggest that the neutrophil-induced ATP depletion in Daudi cells is HOCl-dependent, is not mediated by NH2Cl or TauNHCl, and could be promoted either by HOCl directly or by an unknown derivative oxidant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil-induced depletion of adenosine triphosphate in target cells: evidence for a hypochlorous acid-mediated process. 284 84