9-Hydroxybenfluron: cytostatic effects and inhibition of macromolecular biosynthesis in Ehrlich ascites and P388 murine leukemia cells.

Abstract

Primary screening in vitro and study on the mode of action of 9-hydroxybenfluron (HBF) in both murine P388 leukemia and Ehrlich ascites carcinoma cells have been performed. Metabolite HBF is approximately twice as effective as a reference drug (benfluron). To elucidate the biochemical mode of action, the effect of HBF on the biosynthesis of macromolecules indicated by the incorporation rate of [14C]adenine (in DNA and RNA), [14C]thymidine (in DNA), [14C]uridine (in RNA) and [14C]valine (in protein) was studied in concentration and time dependence. HBF inhibited incorporation of all four precursors into the trichloroacetic acid-insoluble fraction of Ehrlich ascites cells. The fact that incorporation of these four precursors is inhibited suggests that the effect of HBF lies at an underlying level of energy generation or transfer rather than at specific reactions in the biosynthesis of DNA and proteins.

• Authors: M Miko, J Krepelka, M Melka
• Journal: Anti-cancer drugs (Anticancer Drugs) Vol. 2 Issue 3 Pg. 289-95 (Jun 1991) ISSN: 0959-4973 [Print] England
• PMID: 1802025 (Publication Type: Journal Article)

Chemical References

• Antineoplastic Agents
• DNA, Neoplasm
• Fluorenes
• Neoplasm Proteins
• RNA, Neoplasm
• 9-hydroxybenfluron
• Valine
• Adenine
• Thymidine
• Uridine

Topics

• Adenine (metabolism)
• Animals
• Antineoplastic Agents (pharmacology, therapeutic use)
• Carcinoma, Ehrlich Tumor (drug therapy, metabolism)
• DNA, Neoplasm (biosynthesis)
• Fluorenes (pharmacology)
• Leukemia P388 (drug therapy, metabolism)
• Mice
• Mice, Inbred Strains
• Neoplasm Proteins (biosynthesis)
• RNA, Neoplasm (biosynthesis)
• Thymidine (metabolism)
• Tumor Cells, Cultured (drug effects, metabolism)
• Uridine (metabolism)
• Valine (metabolism)