Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-Inhibitors
Teleocidin (5 μg/mouse), a potent tumor promoting indole alkaloid from Streptomyces, 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 p-bromophenacyl...
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| Veröffentlicht in: | Japanese journal of pharmacology 1985, Vol.37(3), pp.253-258 |
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| container_title | Japanese journal of pharmacology |
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| creator | NAKADATE, Teruo AIZU, Eriko YAMAMOTO, Satoshi FUJIKI, Hirota SUGIMURA, Takashi KATO, Ryuichi |
| description | Teleocidin (5 μg/mouse), a potent tumor promoting indole alkaloid from Streptomyces, 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 p-bromophenacyl bromide (BPB) (30 μmol/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 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 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. |
| doi_str_mv | 10.1254/jjp.37.253 |
| format | Article |
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Teleocidin-caused ODC induction was inhibited by the treatment of indomethacin (2 μmol/mouse), a selective cyclooxygenase inhibitor, and p-bromophenacyl bromide (BPB) (30 μmol/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 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 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.</description><identifier>ISSN: 0021-5198</identifier><identifier>EISSN: 1347-3506</identifier><identifier>DOI: 10.1254/jjp.37.253</identifier><identifier>PMID: 3923244</identifier><identifier>CODEN: JJPAAZ</identifier><language>eng</language><publisher>Kyoto: The Japanese Pharmacological Society</publisher><subject>Animals ; Arachidonic Acid ; Arachidonic Acids - metabolism ; Biological and medical sciences ; Carcinogens - pharmacology ; Cyclooxygenase Inhibitors ; Enzyme Induction - drug effects ; Epidermis - enzymology ; Female ; General aspects ; Lipoxygenase Inhibitors ; Lyngbya Toxins - antagonists & inhibitors ; Medical sciences ; Mice ; Ornithine Decarboxylase - biosynthesis ; Phospholipases A - antagonists & inhibitors ; Phospholipases A2 ; Tumors</subject><ispartof>The Japanese Journal of Pharmacology, 1985, Vol.37(3), pp.253-258</ispartof><rights>The Japanese PharmacologicalSociety</rights><rights>1986 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8411753$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3923244$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAKADATE, Teruo</creatorcontrib><creatorcontrib>AIZU, Eriko</creatorcontrib><creatorcontrib>YAMAMOTO, Satoshi</creatorcontrib><creatorcontrib>FUJIKI, Hirota</creatorcontrib><creatorcontrib>SUGIMURA, Takashi</creatorcontrib><creatorcontrib>KATO, Ryuichi</creatorcontrib><title>Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-Inhibitors</title><title>Japanese journal of pharmacology</title><addtitle>Jpn.J.Pharmacol.</addtitle><description>Teleocidin (5 μg/mouse), a potent tumor promoting indole alkaloid from Streptomyces, 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 p-bromophenacyl bromide (BPB) (30 μmol/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 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 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.</description><subject>Animals</subject><subject>Arachidonic Acid</subject><subject>Arachidonic Acids - metabolism</subject><subject>Biological and medical sciences</subject><subject>Carcinogens - pharmacology</subject><subject>Cyclooxygenase Inhibitors</subject><subject>Enzyme Induction - drug effects</subject><subject>Epidermis - enzymology</subject><subject>Female</subject><subject>General aspects</subject><subject>Lipoxygenase Inhibitors</subject><subject>Lyngbya Toxins - antagonists & inhibitors</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Ornithine Decarboxylase - biosynthesis</subject><subject>Phospholipases A - antagonists & inhibitors</subject><subject>Phospholipases A2</subject><subject>Tumors</subject><issn>0021-5198</issn><issn>1347-3506</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU1PwzAMhiMEGmNw4Y6UA0c68tW1PaJuwKRJ4zDOlZuka6ourZJNoj-C_0xg07jYsp9X1msboXtKppTF4rlp-ilPpizmF2hMuUgiHpPZJRoTwmgU0yy9RjfeN6FMCRUjNOIZ40yIMfpe2tqUZm86i7sKb3SrO2mUsVEOB68VXvRGabeDFq-dNfvaWI3nWoIru6-hBa_x0qqD_BtQDvij7nxfd63pf9ELi55wPsi2C-KttqEXYbAKr0z_3zlZ6Jy_RVcVtF7fnfIEfb4uNvl7tFq_LfOXVdQE0yKiSqtSpALCMiWwOCspYRmhiYSYgWScC0F0UmVSkWA1VHSmmUyTcBpIM-AT9HCc2x_KnVZF78wO3FCczhL444mDl9BWDqw0_ixLBaVJzINsfpQ1fg9bfebg9ka2umj62tMspgVPCn4M4UdnLGtwhbb8Bx0Lisw</recordid><startdate>1985</startdate><enddate>1985</enddate><creator>NAKADATE, Teruo</creator><creator>AIZU, Eriko</creator><creator>YAMAMOTO, Satoshi</creator><creator>FUJIKI, Hirota</creator><creator>SUGIMURA, Takashi</creator><creator>KATO, Ryuichi</creator><general>The Japanese Pharmacological Society</general><general>Japanese Pharmacological Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>1985</creationdate><title>Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-Inhibitors</title><author>NAKADATE, Teruo ; AIZU, Eriko ; YAMAMOTO, Satoshi ; FUJIKI, Hirota ; SUGIMURA, Takashi ; KATO, Ryuichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j2444-1dedb484a014ba259b1029017ca52ac233440e7f9cd0eca34416e2c87347a89a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>Arachidonic Acid</topic><topic>Arachidonic Acids - metabolism</topic><topic>Biological and medical sciences</topic><topic>Carcinogens - pharmacology</topic><topic>Cyclooxygenase Inhibitors</topic><topic>Enzyme Induction - drug effects</topic><topic>Epidermis - enzymology</topic><topic>Female</topic><topic>General aspects</topic><topic>Lipoxygenase Inhibitors</topic><topic>Lyngbya Toxins - antagonists & inhibitors</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Ornithine Decarboxylase - biosynthesis</topic><topic>Phospholipases A - antagonists & inhibitors</topic><topic>Phospholipases A2</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>NAKADATE, Teruo</creatorcontrib><creatorcontrib>AIZU, Eriko</creatorcontrib><creatorcontrib>YAMAMOTO, Satoshi</creatorcontrib><creatorcontrib>FUJIKI, Hirota</creatorcontrib><creatorcontrib>SUGIMURA, Takashi</creatorcontrib><creatorcontrib>KATO, Ryuichi</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Japanese journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKADATE, Teruo</au><au>AIZU, Eriko</au><au>YAMAMOTO, Satoshi</au><au>FUJIKI, Hirota</au><au>SUGIMURA, Takashi</au><au>KATO, Ryuichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-Inhibitors</atitle><jtitle>Japanese journal of pharmacology</jtitle><addtitle>Jpn.J.Pharmacol.</addtitle><date>1985</date><risdate>1985</risdate><volume>37</volume><issue>3</issue><spage>253</spage><epage>258</epage><pages>253-258</pages><issn>0021-5198</issn><eissn>1347-3506</eissn><coden>JJPAAZ</coden><abstract>Teleocidin (5 μg/mouse), a potent tumor promoting indole alkaloid from Streptomyces, 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 p-bromophenacyl bromide (BPB) (30 μmol/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 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 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.</abstract><cop>Kyoto</cop><pub>The Japanese Pharmacological Society</pub><pmid>3923244</pmid><doi>10.1254/jjp.37.253</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Japanese Journal of Pharmacology, 1985, Vol.37(3), pp.253-258 |
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| subjects | Animals Arachidonic Acid Arachidonic Acids - metabolism Biological and medical sciences Carcinogens - pharmacology Cyclooxygenase Inhibitors Enzyme Induction - drug effects Epidermis - enzymology Female General aspects Lipoxygenase Inhibitors Lyngbya Toxins - antagonists & inhibitors Medical sciences Mice Ornithine Decarboxylase - biosynthesis Phospholipases A - antagonists & inhibitors Phospholipases A2 Tumors |
| title | Inhibition of Teleocidin-Caused Epidermal Ornithine Decarboxylase Induction by Phospholipase A2-, Cyclooxygenase- and Lipoxygenase-Inhibitors |
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