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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Comparative Biochemistry and Physiology -- Part B: Biochemistry and 46 (1973), S. 639-641 
    ISSN: 0305-0491
    Keywords: Reduced glutathione ; cattle ; dromedary ; erythrocytes ; glutathione reductase ; guinea pig ; man ; rabbit ; rat ; sheep
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism 239 (1971), S. 267-272 
    ISSN: 0005-2760
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 275 (1972), S. 203-211 
    ISSN: 1432-1912
    Keywords: Glutathione Reductase ; Glutathione ; Haemolysis ; Direct Lytic Factor ; Disulphides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The activity of glutathione reductase (GR) was measured in haemolysates and red cell membranes of various species. The enzyme levels were compared with the susceptibility of the respective cells to the direct lytic factor (DLF) of cobra venom. A positive correlation was found in so far as cells having high (low) GR activity were highly (little) sensitive to DLF. Further results make it likely that GR is implicated in DLF-induced lysis: 1. By enzymatic assay an interaction of membrane bound GR and DLF was found, as evident from consumption of the coenzyme NADPH. 2. Glutathione in the reduced state (GSH) as well as in the oxidized form (GSSG) inhibited haemolysis by DLF in a dose-dependent manner. A chemical interaction between DLF and glutathione was excluded. 3. NADPH showed a dual effect: it accelerated DLF-induced haemolysis at low concentrations, whereas at high concentrations inhibition was evident.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1912
    Keywords: Histamine ; Prostaglandin ; Mast Cells ; Cobra Venom ; Phospholipase A ; Direct Lytic Factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of Direct Lytic Factor (DLF) and phospholipase A (ph-ase A) from cobra venom, alone and in combination, on mast cell degranulation, histamine release and formation of prostaglandin-like activity (SRS-C) was studied in perfused guinea-pig lungs and in mast cell-containing rat peritoneal cell suspensions. For comparison, the effect of equivalent doses of whole cobra venom was investigated. 1. Cobra venom caused mast cell degranulation, histamine release and SRS-C formation in both systems. For comparable effects much higher doses had to be used in guinea-pig lungs than in rat peritoneal cell suspensions. 2. Ph-ase A showed little degranulation of mast cells in both systems, a limited histamine release in rat peritoneal cell suspensions and none in perfused guinea-pig lungs. It caused a considerable SRS-C formation in both, lung tissue and peritoneal cell suspensions. 3. DLF caused histamine release, SRS-C formation and mast cell degranulation in both systems; in rat peritoneal cell suspensions it acted almost as strong as equivalent doses of cobra venom, in guinea pig lungs it was much less active. 4. In rat peritoneal cell suspensions the effects of DLF and ph-ase A in combination did not exceed the sum of their single effects. In guinea-pig lungs these two substances interacted in a potentiating synergism. It is concluded that DLF is the main cytotoxic principle of cobra venom, whereas ph-ase A alone is not cytotoxic. The difference in the synergism of DLF and ph-ase A between rat peritoneal cells and guinea-pig lungs may be due to two different actions of DLF and species differences as regards sensitivity against these actions.
    Type of Medium: Electronic Resource
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