Consequences of Cell Membrane Attack by Complement: Release of Arachidonate and Formation of Inflammatory Derivatives

Treatment of [3H]arachidonic acid ([3H]C20:4)-labeled and antibody-sensitized Ehrlich ascites tumor cells with guinea pig or rabbit serum complement (C) released up to about 20 or 25% of the incorporated [3H]C20:4 into the aqueous phase as a consequence of C-induced hydrolysis of cellular phospholip...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1983-11, Vol.80 (21), p.6647-6651
Main Authors: Imagawa, David K., Osifchin, Nicole E., Paznekas, William A., Shin, Moon L., Mayer, Manfred M.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Arachidonic Acid
Arachidonic Acids - metabolism
Carcinoma, Ehrlich Tumor - physiopathology
Cell death
Cell Survival
Complement Membrane Attack Complex
Complement System Proteins - physiology
Cytotoxicity, Immunologic
Dose response relationship
Dose-Response Relationship, Immunologic
Humans
Lipids
Macrophages
Macrophages - physiology
Membrane Lipids - metabolism
Mice
Peritoneal macrophages
Phosphatidic acids
Phospholipases - metabolism
Phospholipids
Reed Sternberg cells
Solvents
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Summary:Treatment of [3H]arachidonic acid ([3H]C20:4)-labeled and antibody-sensitized Ehrlich ascites tumor cells with guinea pig or rabbit serum complement (C) released up to about 20 or 25% of the incorporated [3H]C20:4 into the aqueous phase as a consequence of C-induced hydrolysis of cellular phospholipid. The dose--response curve of release of [3H]C20:4 from Ehrlich ascites tumor cells, with respect to C, was approximately in the same range as the cytolytic response. In the case of [3H]C20:4-labeled and antibody-sensitized peritoneal mouse macrophages, treatment with C induced release of about 11% of the incorporated3H as C20:4 and about 6% as prostaglandins, thromboxane B2, and hydroxyicosatetraenoic acids. C6- and C8-deficient rabbit and human sera, respectively, induced release of small amounts of [3H]C20:4 from Ehrlich ascites tumor cells and macrophages; these deficient sera also released traces of oxygenated derivatives from macrophages. Addition of purified C6 or C8 effectively restored release from both cell types, indicating that the terminal C proteins, up to and including C8, are required for the major part of the release. Our results do not rule out a possible requirement for C9.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.80.21.6647