Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-lnhibitors

Teruo Nakadate, Eriko Aizu, Satoshi Yamamoto, Ryuichi Kato

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Teleocidin (5µg/mouse), a potent tumor promoting indole alkaloid from Streptomyces, induced epidermal ornithine decarboxylase (ODC) in CD-I mice. Teleocidin-caused ODC induction was inhibited by the treatment of indo-methacin (2µmol/mouse), a selective cyclooxygenase inhibitor, and p-bromo-phenacyl bromide (BPB) (30µmol/mouse), a phospholipase A2 inhibitor. Teleocidin-caused ODC induction inhibited by indomethacin was completely restored by concurrent application of prostaglandin E2 (PGE2) (140 nmol/mouse). On the other hand, teleocidin-caused ODC induction inhibited by BPB was not restored by the treatment of mice with PGE2, but partially restored by the treatment with arachidonic acid (1 //mol/mouse). Treatment of mice with lipoxygenase inhibitors such as BW755C (30µmol/mouse), nordihydroguaiaretic acid (NDGA) (30µmol/mouse), quercetin (10µmol/mouse), and 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-l, 4-benzoquinone (AA861) (10 /imol/mouse) clearly suppressed ODC induction by teleocidm. Moreover, both NDGA (30µmol/mouse) and quercetin (10µmol/mouse) inhibited the restoring effect of PGE2. Therefore, our present results suggest that arachidonate metabolites, i.e., not only cyclooxygenase product(s) but also lipoxygenase product(s), are involved in the mechanism of ODC induction by teleocidin.

Original languageEnglish
Pages (from-to)253-258
Number of pages6
JournalThe Japanese Journal of Pharmacology
Volume37
Issue number3
DOIs
Publication statusPublished - 1985

ASJC Scopus subject areas

  • Pharmacology

Fingerprint Dive into the research topics of 'Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-lnhibitors'. Together they form a unique fingerprint.

  • Cite this