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Biological Trace Element Research

, Volume 154, Issue 2, pp 268–274 | Cite as

The Alteration of Copper Homeostasis in Inflammation Induced by Lipopolysaccharides

  • Ming HanEmail author
  • Zhexuan Lin
  • Yuan Zhang
Article

Abstract

Significant changes of copper homeostasis were triggered by lipopolysaccharides, which result in systemic inflammatory response and contribute to hepatic injury. Administration of lipopolysaccharides resulted in the increase of plasma “free” copper and total copper concentrations, whereas, the decrease of “free” copper and total copper contents in liver tissue. Copper-associated proteins were detected and showed a down-regulation of X-linked inhibitor of apoptosis protein, and up-regulation of copper metabolism domain containing 1 and copper transporter 1. The alteration of these proteins would lower the apoptotic threshold. Meanwhile, the increasing of circulation copper might cause oxidative injury through Fenton reaction and contribute to tissue injury. Our findings underscored the possibility that these changes in systemic copper homeostasis might provide a novel insight of the characteristic of the acute phase of inflammatory response and the underlying influence on tissue injury.

Keywords

“Free” copper Total copper Lipopolysaccharides Copper transport associated proteins  

Notes

Acknowledgments

This work is supported by the National Natural Science Foundation of China (project number:81172088), the Joint Scientific Special foundation of Guandong Provincial Department of Science and Technology-Academy of Traditional Chinese Medicine (2012A032500009), and the Natural Science Foundation of Guangdong Province (project number S2012040007604).

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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Second Affiliated Hospital of Shantou University Medical CollegeShantouPeople’s Republic of China
  2. 2.The Key Lab of Molecular Biology for High Cancer Incidence Coastal Chaoshan AreaShantou University Medical CollegeShantouChina

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