Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 7, 2017; 23(41): 7347-7358
Published online Nov 7, 2017. doi: 10.3748/wjg.v23.i41.7347
Reabsorption of iron into acutely damaged rat liver: A role for ferritins
Ihtzaz Ahmed Malik, Jörg Wilting, Giuliano Ramadori, Naila Naz
Ihtzaz Ahmed Malik, Jörg Wilting, Institute of Anatomy and Cell Biology, University Medical Center, D-37075 Goettingen, Germany
Giuliano Ramadori, Department of Gastroenterology and Endocrinology, University Medical Center, D-37075 Goettingen, Germany
Naila Naz, Faculty of Life Sciences, The University of Manchester, Manchester M13 9PL, United Kingdom
Author contributions: Malik IA, Ramadori G and Naz N designed the study; Malik IA and Naz N performed the experiments; Malik IA, Ramadori G and Naz N analyzed the data and wrote manuscript; Wilting J assisted to interpret the data and improved the manuscript; Ramadori G and Naz N contributed equally to this work.
Supported by the German Research Foundation, and the Open Access Publication Funds of the Göttingen University.
Institutional review board statement: The studies were performed according to the guidelines of good scientific practice.
Institutional animal care and use committee statement: The animal studies were reviewed and approved by the committee of the Central Institute for Animal Experiments of the University of Goettingen, and the Lower Saxony State Office for Consumer Protection and Food Safety (Study No. 33.9-42502-04-13/1086).
Conflict-of-interest statement: The authors declare that no actual or potential conflict-of-interest in relation to this article exists.
Data sharing statement: The data were obtained, analyzed and used by the authors only.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ihtzaz Ahmed Malik, PhD, Institute of Anatomy and Cell Biology, University Medical Center Goettingen, Kreuzbergring 36, D-37075 Goettingen, Germany. i.malik@med.uni-goettingen.de
Telephone: +49-551-398982 Fax: +49-551-397067
Received: July 16, 2017
Peer-review started: July 21, 2017
First decision: August 10, 2017
Revised: August 22, 2017
Accepted: September 13, 2017
Article in press: September 13, 2017
Published online: November 7, 2017
Core Tip

Core tip: In humans, an increase in hepatic iron concentration is caused by chronic hepatitis-C infection, alcohol abuse, and non-alcoholic fatty liver disease. The pathophysiology behind increased liver iron concentrations caused by acute liver damage has remained obscure. Using thioacetamide-injection in rats, we demonstrate that the increase in liver iron may be a consequence rather than the cause of hepatocyte damage. Thereby, iron is released into serum by damaged hepatocytes during acute liver damage, and reabsorbed by remaining hepatocytes (but not spleen) by means of ferritin L and ferritin H subunits. Our studies also show that ferritin H is a promising surrogate marker for damaged hepatocytes.