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)

In the present paper, the involvement of active oxygen species in bone resorption has been studied. In order to compare the production of active oxygen by mouse marrow culture cells, fluorescence due to peroxides reacted with 2,7-dichlorofluorescin was measured. After marrow cells were cultured with 1,25-(OH)2D3 for 8 days, there were tartrate resistant acid phosphatase positive multinucleated cells (TRACP(+)MNCs), TRACP positive mononucleated cells, macrophage-like cells and marrow derived stromal cells. Among these cells, TRACP(+) cells could produce almost the equivalent amount of peroxides as could the macrophage-like cells. In order to examine the role of active oxygen in bone metabolism, the amount of oxidative stress was altered during the culture period in the same marrow culture system. Catalase, a catabolic enzyme of hydrogen peroxide (H2O2), significantly suppressed the formation of TRACP(+)MNCs in a dose dependent manner. This suppression was limited in the early stage of the culture period and was reduced by the addition of exogenous H2O2 to culture. Moreover, when superoxide dismutase, a converting enzyme from superoxide anion to H2O2, was added in this system, the formation of TRACP(+)MNCs was significantly increased. These results strongly suggest that active oxygen species, especially H2O2, may be involved in the regulation of osteoclast formation.
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PMID:Participation of oxidative stress in the process of osteoclast differentiation. 832 62

Iron-containing proteins catalyze lipid peroxidation when combined with either H2O2 or ascorbic acid (ASC). Microsomal membranes were prepared from Day 13 endometrial and conceptus tissues (5 pigs) and from Day 30 endometrial, placental, fetal liver, and fetus minus fetal liver tissues (5 pigs). Microsomal membranes were subjected to the following in vitro treatments: 1) no treatment, 2) 50 microM ASC, 3) 100 microM uteroferrin (UF), 4) 50 microM ASC + 100 microM UF, 5) 50 microM ASC + 100 microM UF + 10 microM apotransferrin (transferrin with no iron bound; ATF), and 6) 50 microM ASC + 100 microM UF + 10 microM holotransferrin (transferrin saturated with iron; HTF). For treatments 7 through 10, membranes were preincubated (0 degrees C, 3 h) with either 7) no treatment, 8) 50 microM fetuin, 9) 50 microM holoretinol binding protein (holoRBP: retinol binding protein [HoloRBP] with retinol bound), or 10) 50 microM apoRBP (RBP with no retinol bound) followed by incubation with 50 microM ASC + 100 microM UF. Lipid peroxidation was measured in the samples as thiobarbituric acid reactive substances (TBARS). Endogenous TBARS were greater (p < 0.05) in Day 13 conceptus than in Day 13 endometrium and were highest (p < 0.05) on Day 30 in fetal liver. Combined ASC and UF caused a large increase (p < 0.05) in TBARS in all membranes except Day 30 placental membranes. Addition of ATF, but not HTF, decreased TBARS production in all membrane preparations. HoloRBP, but not fetuin or apoRBP, decreased (p < 0.05) TBARS production in all but Day 30 endometrial membranes. In other experiments, when combined with ASC, UF/UF-associated protein complex induced less (p < 0.01) lipid peroxidation in fetal liver microsomal membranes than did free UF. Catalase and superoxide dismutase had no effect on UF-induced lipid peroxidation in fetal liver membranes. These results indicate that 1) UF combined with ASC induces lipid peroxidation in Day 13 endometrial and conceptus and Day 30 endometrial, fetal liver, and fetus minus liver microsomal membranes, and 2) ATF, holoRBP, and the UF-associated proteins, but not catalase or superoxide dismutase, inhibit this reaction.
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PMID:Uteroferrin induces lipid peroxidation in endometrial and conceptus microsomal membranes and is inhibited by apotransferrin, retinol binding protein, and the uteroferrin-associated proteins. 856 1