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)

I examined the effects of host cells reactive to foreign bodies such as plastic plate or hemostatic spongel on the progression of tumor cells. QR tumor cells spontaneously regressed in normal C57BL/6 mice apparently associated with a reduction in production of PGE2 by the tumor cells. I have observed that such regressor tumor cells are able to grow lethally when implanted in mice after having been attached to plastic plate. The clones which were derived from these plastic plate-derived tumors in normal mice maintained their growth potential when they were injected into other normal mice. Furthermore the arising tumors produce much higher levels of PGE2 than the original QR tumor cells. Interestingly, I could not observe acquisition of tumorigenicity or a higher level of PGE2-production in the clones obtained from the arising tumors which were grown in 10Gy-irradiated mice. Moreover, QR tumor cells are able to grow in mice when they are injected at the site where plastic plate had been implanted about 30 days previously. These results indicate that the restoration of tumorigenicity of QR tumor cells is not only due to attachment to plastic plate, but also mediated by radiation-sensitive host cells reactive to plastic plate which enhance the progression of tumor cells. Similar results are also obtained by coinoculation of QR tumor cells with host reactive cells which had been induced by implantation of hemostatic spongels into the peritoneal cavity of mice. Greater amounts of PGE2-production by QR tumor cells were observed when the tumor cells were cocultured with spongel reactive cells. This PGE2-production was markedly inhibited by the presence of radical scavengers (Catalase, Mannitol, SOD + Catalase) in the coculture medium(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Progression of regressor tumor cells by host reactive cells to such foreign bodies as plastic plate and hemostatic spongel]. 237 14

Macrophage-mediated suppression of Con A induced proliferation of murine splenic lymphocytes was studied in vitro. Either Corynebacterium parvrum-induced peritoneal exudate cells (PEC) or thioglycollate-induced PEC could totally suppress lymphocyte proliferation at a PEC:lymphocyte ratio of 2:10, whereas a ratio of 1 to 1.5: 10 caused a partial (60 to 68%) suppression. Exogenous PGE1 and PGE2 at concentrations of 10(-8) to 10(-6) M could not totally suppress lymphocyte proliferation. Conversely, indomethacin reversed the partial suppression by macrophages but only partially protected the totally suppressed lymphocyte cultures. Macrophage-mediated cytotoxicity and cytostasis have been proposed to be mediated by hydrogen peroxide. Therefore, hydrogen peroxide was investigated as a possible additional cause for macrophage-mediated suppression, by testing the anti-inhibitory effects of catalase. Partially suppressed cultures were effectively protected from suppression by catalase. In totally suppressed cultures, catalase alone was only minimally effective, but a synergistic effect of catalase and indomethacin was obtained, which provided complete protection from maximal macrophage-mediated suppression. Catalase presumably contributes to the reversal of macrophage suppressive effects both by reducing the direct toxic effect of H2O2 and by preventing the H2O2 from generating additional prostaglandins.
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PMID:Macrophage-mediated suppression. I. Evidence for participation of both hdyrogen peroxide and prostaglandins in suppression of murine lymphocyte proliferation. 735 24

This study was performed to clarify the mechanism of vasoconstriction induced by oxygen-derived free radicals in spontaneously hypertensive rats. The isometric tension of aortic rings from spontaneously hypertensive rats and Wistar-Kyoto rats was measured in Krebs-Henseleit solution. Oxygen-derived free radicals were generated by mixing xanthine and xanthine oxidase. The removal of endothelium enhanced the contractions induced by oxygen-derived free radicals. The inhibition of nitric oxide production with NG-nitro-L-arginine methyl ester (10(-4) M) enhanced the contractions. Treatment with the thromboxane A2 (TXA2) synthetase inhibitor OKY-046 (10(-4) M) or RS-5186 (10(-4) M) markedly reduced the contractions. Treatment with the cyclooxygenase inhibitor indomethacin (10(-5) M) and a TXA2/prostaglandin H2 (PGH2) receptor antagonist, ONO-3708 (10(-6) M), completely abolished the oxygen-derived free radical-induced contractions. In contrast, treatment with the PGI2 synthetase inhibitor tranylcypromine (10(-4) M) did not attenuate the oxygen-derived free radical-induced contractions. Whether endothelium was present or not, the release of TXB2, PGE2, and 6-keto-PGF1alpha, but not PGF2alpha, was increased by the production of oxygen-derived free radicals. Catalase and the hydroxyl radical scavenger deferoxamine plus mannitol markedly inhibited the oxygen-derived free radical-induced contractions. These results suggest that oxygen-derived free radical-induced vasoconstriction in spontaneously hypertensive rat aorta is caused by TXA2 and PGH2 released in smooth muscle.
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PMID:Oxygen-derived free radical-induced vasoconstriction by thromboxane A2 in aorta of the spontaneously hypertensive rat. 1021 31