2. Academic Validation
  3. Serum iron increases with acute induction of hepatic heme oxygenase-1 in mice

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

  • Drug Metab Rev. 2007;39(2-3):619-26. doi: 10.1080/03602530701468342.
Volker Mostert 1,  Akihiro Nakayama,  Lori M Austin,  Ximena A Levander,  Christopher D Ferris,  Kristina E Hill,  Raymond F Burk
Affiliations

Affiliation

  • 1 Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
PMID: 17786642 DOI: 10.1080/03602530701468342
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.

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