Serum iron increases with acute induction of hepatic heme oxygenase-1 in mice

Volker Mostert, Akihiro Nakayama, Lori M. Austin, Ximena A. Levander, Christopher D. Ferris, Kristina E. Hill, Raymond F. Burk

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)619-626
Number of pages8
JournalDrug Metabolism Reviews
Issue number2-3
StatePublished - Apr 2007
Externally publishedYes


  • Heme
  • Heme oxygenase-1
  • Heme synthesis
  • Iron export
  • Oxidative stress
  • Selenium deficiency

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Pharmacology (medical)


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