Effect of RU 38486 on TNF production and toxicity

George Lázár, Ernö Duda, George Lázár

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Gluracarticoid steroids provide considerable protection against the systemic toxicity or tumor necrosis factor-α (TNF-α, cachexin). In animal experiments RU 38486 (mircpristone), a steroid antagonist, increased the synthesis of TNF and sensitized the animals to the cytotoxic action of TNF. As compared to the control and methylprednisolone-treated groups, mifepristone significantly increased the level of TNF in the serum, liver and spleen or lipopolysaccharide (LPS)-treated animals. In tissue cultures F.U. 38486 induced the TNF synthesis of mycloid cells and increase the TNF production or genetically modified HeLa cells, which synthesize TNF constitutively. Normal and tumor cell cultures exhibited increased sensitivity toward TNF in the presence of mifepristone.

Original languageEnglish
Pages (from-to)137-140
Number of pages4
JournalFEBS letters
Volume308
Issue number2
DOIs
Publication statusPublished - Aug 17 1992

Keywords

  • Endotoxin
  • Glucocorticoid
  • Mifeprisone
  • RU 38486
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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