Gunshin Hiromi, Starr Carolyn N, Direnzo Cristina, Fleming Mark D, Jin Jie, Greer Eric L, Sellers Vera M, Galica Stephanie M, Andrews Nancy C
Children's Hospital, Karp Family Research Laboratories RM 8-125, Boston, MA 02115-5737, USA.
Blood. 2005 Oct 15;106(8):2879-83. doi: 10.1182/blood-2005-02-0716. Epub 2005 Jun 16.
Mammalian nonheme iron absorption requires reduction of dietary iron for uptake by the divalent metal ion transport system in the intestine. This was thought to be mediated by duodenal cytochrome b (Cybrd1), a ferric reductase enzyme resident on the luminal surface of intestinal absorptive cells. To test its importance in vivo, we inactivated the murine Cybrd1 gene and assessed tissue iron stores in Cybrd1-null mice. We found that loss of Cybrd1 had little or no impact on body iron stores, even in the setting of iron deficiency. We conclude that other mechanisms must be available for the reduction of dietary iron.
哺乳动物非血红素铁的吸收需要将膳食铁还原,以便通过肠道中的二价金属离子转运系统进行摄取。这一过程曾被认为是由十二指肠细胞色素b(Cybrd1)介导的,它是一种存在于肠道吸收细胞腔表面的铁还原酶。为了测试其在体内的重要性,我们使小鼠的Cybrd1基因失活,并评估了Cybrd1基因缺失小鼠的组织铁储备。我们发现,即使在缺铁的情况下,Cybrd1的缺失对机体铁储备几乎没有影响。我们得出结论,必然存在其他机制来还原膳食铁。