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

被引：6

作者：

Mostert, Volker ^{[1
]}

Nakayama, Akihiro ^{[1
]}

Austin, Lori M. ^{[1
]}

Levander, Ximena A. ^{[1
]}

Ferris, Christopher D. ^{[1
]}

Hill, Kristina E. ^{[1
]}

Burk, Raymond F. ^{[1
]}

机构：

[1] Vanderbilt Univ, Dept Med, Sch Med, Div Gastroenterol Hepatol & Nutr, Nashville, TN 37232 USA

来源：

DRUG METABOLISM REVIEWS | 2007年 / 39卷 / 2-3期

关键词：

heme synthesis; heme oxygenase-1; iron export; oxidative stress; selenium deficiency; heme; SELENIUM-DEFICIENT RATS; OXIDATIVE STRESS; INHIBITION; BRAIN; GENE;

D O I：

10.1080/03602530701468342

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

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-triinetityl-3,5-pyriditiedicarboxylate (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.

引用

页码：619 / 626

页数：8

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