Serum iron increases with acute induction of hepatic heme oxygenase-1 in mice
Heme oxygenase (HO)-1 is induced by oxidative stress and protects against oxidant injury. We examined the effect of rapid induction of hepatic HO-1 on serum iron level. Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice. Blocki...
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| Veröffentlicht in: | Drug metabolism reviews 2007-01, Vol.39 (2-3), p.619-626 |
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| container_title | Drug metabolism reviews |
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| creator | MOSTERT, Volker NAKAYAMA, Akihiro AUSTIN, Lori M LEVANDER, Ximena A FERRIS, Christopher D HILL, Kristina E BURK, Raymond F |
| description | Heme oxygenase (HO)-1 is induced by oxidative stress and protects against oxidant injury. We examined the effect of rapid induction of hepatic HO-1 on serum iron level. Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice. Blocking heme synthesis with diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) prevented the induction of HO-1 and the rise in serum iron. DDC did not block HO-1 induction by hemin. Inhibition of HO activity by tin protoporphyrin prevented a rise in serum iron that occurred following phorone treatment. These results indicate that heme synthesis or an exogenous source of heme is needed to allow induction of HO-1. Further, they link HO-1 induction with a rise in serum iron, suggesting that the iron resulting from catabolism of heme by HO-1 is released by the liver. |
| doi_str_mv | 10.1080/03602530701468342 |
| format | Article |
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We examined the effect of rapid induction of hepatic HO-1 on serum iron level. Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice. Blocking heme synthesis with diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) prevented the induction of HO-1 and the rise in serum iron. DDC did not block HO-1 induction by hemin. Inhibition of HO activity by tin protoporphyrin prevented a rise in serum iron that occurred following phorone treatment. These results indicate that heme synthesis or an exogenous source of heme is needed to allow induction of HO-1. Further, they link HO-1 induction with a rise in serum iron, suggesting that the iron resulting from catabolism of heme by HO-1 is released by the liver.</description><identifier>ISSN: 0360-2532</identifier><identifier>EISSN: 1097-9883</identifier><identifier>DOI: 10.1080/03602530701468342</identifier><identifier>PMID: 17786642</identifier><identifier>CODEN: DMTRAR</identifier><language>eng</language><publisher>New York, NY: Informa Healthcare</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Dihydropyridines - pharmacology ; Enzyme Induction - drug effects ; Enzyme Induction - physiology ; Heme - antagonists & inhibitors ; Heme - biosynthesis ; Heme Oxygenase-1 - biosynthesis ; Iron - blood ; Liver - drug effects ; Liver - enzymology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Pharmacology. 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We examined the effect of rapid induction of hepatic HO-1 on serum iron level. Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice. Blocking heme synthesis with diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) prevented the induction of HO-1 and the rise in serum iron. DDC did not block HO-1 induction by hemin. Inhibition of HO activity by tin protoporphyrin prevented a rise in serum iron that occurred following phorone treatment. These results indicate that heme synthesis or an exogenous source of heme is needed to allow induction of HO-1. Further, they link HO-1 induction with a rise in serum iron, suggesting that the iron resulting from catabolism of heme by HO-1 is released by the liver.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Dihydropyridines - pharmacology</subject><subject>Enzyme Induction - drug effects</subject><subject>Enzyme Induction - physiology</subject><subject>Heme - antagonists & inhibitors</subject><subject>Heme - biosynthesis</subject><subject>Heme Oxygenase-1 - biosynthesis</subject><subject>Iron - blood</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Selenium - deficiency</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MOSTERT, Volker</creatorcontrib><creatorcontrib>NAKAYAMA, Akihiro</creatorcontrib><creatorcontrib>AUSTIN, Lori M</creatorcontrib><creatorcontrib>LEVANDER, Ximena A</creatorcontrib><creatorcontrib>FERRIS, Christopher D</creatorcontrib><creatorcontrib>HILL, Kristina E</creatorcontrib><creatorcontrib>BURK, Raymond F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Drug metabolism reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MOSTERT, Volker</au><au>NAKAYAMA, Akihiro</au><au>AUSTIN, Lori M</au><au>LEVANDER, Ximena A</au><au>FERRIS, Christopher D</au><au>HILL, Kristina E</au><au>BURK, Raymond F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum iron increases with acute induction of hepatic heme oxygenase-1 in mice</atitle><jtitle>Drug metabolism reviews</jtitle><addtitle>Drug Metab Rev</addtitle><date>2007-01-01</date><risdate>2007</risdate><volume>39</volume><issue>2-3</issue><spage>619</spage><epage>626</epage><pages>619-626</pages><issn>0360-2532</issn><eissn>1097-9883</eissn><coden>DMTRAR</coden><abstract>Heme oxygenase (HO)-1 is induced by oxidative stress and protects against oxidant injury. We examined the effect of rapid induction of hepatic HO-1 on serum iron level. Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice. Blocking heme synthesis with diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) prevented the induction of HO-1 and the rise in serum iron. DDC did not block HO-1 induction by hemin. Inhibition of HO activity by tin protoporphyrin prevented a rise in serum iron that occurred following phorone treatment. These results indicate that heme synthesis or an exogenous source of heme is needed to allow induction of HO-1. Further, they link HO-1 induction with a rise in serum iron, suggesting that the iron resulting from catabolism of heme by HO-1 is released by the liver.</abstract><cop>New York, NY</cop><pub>Informa Healthcare</pub><pmid>17786642</pmid><doi>10.1080/03602530701468342</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Drug metabolism reviews, 2007-01, Vol.39 (2-3), p.619-626 |
| issn | 0360-2532 1097-9883 |
| language | eng |
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| source | MEDLINE; Taylor & Francis Medical Library - CRKN; Taylor & Francis Journals Complete |
| subjects | Animals Biological and medical sciences Blotting, Western Dihydropyridines - pharmacology Enzyme Induction - drug effects Enzyme Induction - physiology Heme - antagonists & inhibitors Heme - biosynthesis Heme Oxygenase-1 - biosynthesis Iron - blood Liver - drug effects Liver - enzymology Male Medical sciences Mice Mice, Inbred C57BL Pharmacology. Drug treatments Selenium - deficiency |
| title | Serum iron increases with acute induction of hepatic heme oxygenase-1 in mice |
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