Copper activates the NF-κB pathway in vivo

Tiziana Persichini, Zulema Percario, Emanuela Mazzon, Marco Colasanti, Salvatore Cuzzocrea, Giovanni Musci

Research output: Contribution to journalArticlepeer-review


Previous results indicated that intravenous injection of copper in the form of a copper-histidine complex in rats triggers the transcriptional induction of the inducible form of nitric oxide synthase (NOS-II). Here, the authors demonstrate that copper activates the transcription factor NF-κB in the liver and lung tissues of rats, and that this effect is mediated by oxidative stress, since all copper-induced changes, which include histological alterations, formation of nitrotyrosines, vascular pressure drop, production of tumor necrosis factor-α (TNF-α), induction of NOS-II and nitrites, are readily prevented by pretreatment of the animals with the antioxidant tempol. By using electrophoretic mobility shift assays, the p50/p65 dimer and higher molecular weight aggregates have been found to be involved in the copper-induced NF-κB activation. COX-2, a NF-κB-dependent gene involved in the inflammatory response, was also transcriptionally induced by copper, this effect being reduced in the presence of tempol. These results suggest that a physiopathological status, characterized by hypercupremic situations, may lead to the onset of inflammation through production of ROS and activation of NF-κB.

Original languageEnglish
Pages (from-to)1897-1904
Number of pages8
JournalAntioxidants and Redox Signaling
Issue number9-10
Publication statusPublished - Sept 2006

ASJC Scopus subject areas

  • Biochemistry


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