Allison Cockrell - Speciation of Iron in Mouse Liver During Development, Iron Deficiency, IRP2 Deletion, and Inflammatory Hepatitis,

Document created by Allison Cockrell Zugell on May 21, 2015
Version 1Show Document
  • View in full screen mode

  Publication Details (including relevant citation   information):

  Mrinmoy Chakrabarti,   Allison L. Cockrell, Jinkyu Park, Sean P.   McCormick, Lora S. Lindahl, and Paul A. Lindahl   (2015) Metallomics 7(1), 93-101


    The iron content of livers from 57Fe-enriched   C57BL/6 mice of different ages were investigated using Mössbauer   spectroscopy, electron paramagnetic resonance (EPR), electronic   absorption spectroscopy and inductively coupled plasma mass   spectrometry (ICP-MS). About 80% of the Fe in an adult liver was   due to blood; thus removal of blood by flushing with buffer was   essential to observe endogenous liver Fe. Even after exhaustive   flushing, ca. 20%   of the Fe in anaerobically dissected livers was typical of   deoxy-hemoglobin. The concentration of Fe in newborn livers was   the highest of any developmental stage ([similar]1.2   mM). Most was stored as ferritin, with little mitochondrial Fe   (consisting primarily of Fe–S clusters and haems) evident. Within   the first few weeks of life, about half of ferritin Fe was   mobilized and exported, illustrating the importance of   Fe release as   well as Fe storage in   liver function. Additional ferritin Fe was used to generate   mitochondrial Fe centres. From ca. 4   weeks of age to the end of the mouse's natural lifespan, the   concentration of mitochondrial Fe in liver was essentially   invariant. A minor contribution from nonhaem high-spin   FeII was   observed in most liver samples and was also invariant with age.   Some portion of these species may constitute the labile iron   pool. Livers from mice raised on an Fe-deficient diet were highly   Fe depleted; they were devoid of ferritin and contained 1/3 as   much mitochondrial Fe as found in Fe-sufficient livers. In   contrast, brains of the same Fe-deficient mice retained normal   levels of mitochondrial Fe. Livers from mice with inflammatory   hepatitis and from IRP2(−/−) mice hyper-accumulated Fe. These   livers had high ferritin levels but low levels of mitochondrial   Fe.

  Address (URL):!divAbstract