Platelet-activating factor antagonists (BN 52021 and BN 50730) inhibit tumor necrosis factor-alfa-mediated cytotoxicity on murine L929 tumor cells

J. Hunyadi, Anna Szabó Kenderessy, E. Duda, Piere Braquet, A. Dobozy

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Tumor necrosis factor (TNF)-alfa has been described as a mononuclear phagocyte-produced cytotoxin that causes the necrosis and regression of some tumors. The mechanism of the cytotoxicity and the basis for the differential cytotoxic effects of TNF against cells of various origin remains unclear. It has also been reported, that murine TNF stimulates the production of platelet-activating factor (PAF) by cultured peritoneal macrophages, and that PAF enhances TNF production by alveolar macrophages. Furthermore, it is known that the synthesis and release of PAF are inhibited by plasma proteinase inhibitors. This study was devoted to investigate the effects of two specific PAF antagonists (BN 52021 and 50730), and a proteinase inhibitor (aprotinin; Gordox R) on the TNF-induced cytotoxicity in L929 murine fibroblasts. Our present findings indicate that TNF-induced cytotoxicity is inhibited in a dose-dependent manner by the PAF antagonists studied and by the kallikrein inhibitor aprotinin. These findings provide further evidence suggesting that PAF might be involved in the process of the TNF-alfa-induced cytotoxicity of L929 mouse fibroblasts.

Original languageEnglish
Pages (from-to)517-519
Number of pages3
JournalMolecular Immunology
Volume30
Issue number6
DOIs
Publication statusPublished - 1993

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ginkgolide B
Platelet Activating Factor
Tumor Necrosis Factor-alpha
Neoplasms
Aprotinin
Peptide Hydrolases
Macrophage-Activating Factors
Fibroblasts
Kallikreins
Cytotoxins
Alveolar Macrophages
Peritoneal Macrophages
Phagocytes
BN 50730

ASJC Scopus subject areas

  • Molecular Biology
  • Immunology

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Platelet-activating factor antagonists (BN 52021 and BN 50730) inhibit tumor necrosis factor-alfa-mediated cytotoxicity on murine L929 tumor cells. / Hunyadi, J.; Kenderessy, Anna Szabó; Duda, E.; Braquet, Piere; Dobozy, A.

In: Molecular Immunology, Vol. 30, No. 6, 1993, p. 517-519.

Research output: Contribution to journalArticle

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AU - Braquet, Piere

AU - Dobozy, A.

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AB - Tumor necrosis factor (TNF)-alfa has been described as a mononuclear phagocyte-produced cytotoxin that causes the necrosis and regression of some tumors. The mechanism of the cytotoxicity and the basis for the differential cytotoxic effects of TNF against cells of various origin remains unclear. It has also been reported, that murine TNF stimulates the production of platelet-activating factor (PAF) by cultured peritoneal macrophages, and that PAF enhances TNF production by alveolar macrophages. Furthermore, it is known that the synthesis and release of PAF are inhibited by plasma proteinase inhibitors. This study was devoted to investigate the effects of two specific PAF antagonists (BN 52021 and 50730), and a proteinase inhibitor (aprotinin; Gordox R) on the TNF-induced cytotoxicity in L929 murine fibroblasts. Our present findings indicate that TNF-induced cytotoxicity is inhibited in a dose-dependent manner by the PAF antagonists studied and by the kallikrein inhibitor aprotinin. These findings provide further evidence suggesting that PAF might be involved in the process of the TNF-alfa-induced cytotoxicity of L929 mouse fibroblasts.

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