Copper accumulates in hemosiderins in livers of patients with iron overload syndromes

Yukiya Ono, Masatoshi Ishigami, Kazuhiko Hayashi, Shinya Wakusawa, Hisao Hayashi, Kotaro Kumagai, Natsuko Morotomi, Tetsuji Yamashita, Miwa Kawanaka, Minemori Watanabe, Hiroaki Ozawa, Mayumi Tai, Hiroaki Miyajima, Kentarou Yoshioka, Yoshiki Hirooka, Hidemi Goto

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

In biology, redox reactions are essential and sometimes harmful, and therefore, iron metabolism is tightly regulated by cuproproteins. Since the state of copper in iron overload syndromes remains unclear, we investigated whether copper metabolism is altered in these syndromes. Eleven patients with iron overload syndromes participated in this study. The clinical diagnoses were aceruloplasminemia (n=2), hemo-chromatosis (n=5), ferroportin disease (n=2), and receiving excess intravenous iron supplementation (n=2). Liver speci-mens were analyzed using a light microscope and transmis-sion electron microscope equipped with an X-ray analyzer. In addition to a large amount of iron associated with oxygen and phosphorus, the iron-rich hemosiderins of hepatocytes and Kupffer cells contained small amounts of copper and sulfur, regardless of disease etiology. Two-dimensional imaging clearly showed that cuproproteins were distributed homoge-nously with iron complexes within hemosiderins. Copper sta-sis was unlikely in noncirrhotic patients. The enhanced induction of cuproproteins by excess iron may contribute to copper accumulation in hemosiderins. In conclusion, we have demonstrated that copper accumulates in hemosiderins in iron overload conditions, perhaps due to alterations in copper metabolism.

Original languageEnglish
Pages (from-to)85-92
Number of pages8
JournalJournal of Clinical and Translational Hepatology
Volume3
Issue number2
DOIs
Publication statusPublished - 2015
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Hepatology

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