Inhibition of teleocidin-caused epidermal ornithine decarboxylase induction by phospholipase A2-, cyclooxygenase- and lipoxygenase-inhibitors.
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概要
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Teleocidin (5 μg/mouse), a potent tumor promoting indole alkaloid from <I>Streptomyces</I>, induced epidermal ornithine decarboxylase (ODC) in CD-1 mice. Teleocidin-caused ODC induction was inhibited by the treatment of indomethacin (2 μmol/mouse), a selective cyclooxygenase inhibitor, and <I>p</I>-bromophenacyl bromide (BPB) (30 μmol/mouse), a phospholipase A<SUB>2</SUB> inhibitor. Teleocidin-caused ODC induction inhibited by indomethacin was completely restored by concurrent application of prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>) (140 nmol/mouse). On the other hand, teleocidin-caused ODC induction inhibited by BPB was not restored by the treatment of mice with PGE<SUB>2</SUB>, but partially restored by the treatment with arachidonic acid (1 μmol/mouse). Treatment of mice with lipoxygenase inhibitors such as BW755C (30 μmol/mouse), nordihydroguaiaretic acid (NDGA) (30 μmol/mouse), quercetin (10 μmol/mouse), and 2, 3, 5-trimethyl-6-(12-hydroxy-5, 10-dodecadiynyl)-1, 4-benzoqu1none (AA861) (10 μmol/mouse) clearly suppressed ODC induction by teleocidin. Moreover, both NDGA (30 μmol/mouse) and quercetin (10 μmol/mouse) inhibited the restoring effect of PGE<SUB>2</SUB>. 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.
- 公益社団法人 日本薬理学会の論文
著者
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SUGIMURA Takashi
National Cancer Center
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Kato Ryuichi
Department Of Biology Graduate School Of Science Osaka University
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Nakadate Teruo
Department Of Chemical Pharmacology Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceut
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Fujiki Hirota
National Cancer Center Research Institute
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Yamamoto Satoshi
Department Of Biochemistry Nagoya University School Of Medicine
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Aizu Eriko
Department of Pharmacology, School of Medicine, Keio University
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SUGIMURA Takashi
National Cancer Center Research Institute
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