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-kappaB 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-alpha (TNF-alpha), 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-kappaB activation. COX-2, a NF-kappaBdependent 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-kappaB.

Persichini, T., Percario, Z.A., Mazzon, E., Colasanti, M., Cuzzocrea, S., Musci, G. (2006). Copper activates the NF-kappaB pathway in vivo. ANTIOXIDANTS & REDOX SIGNALING, 8, 1897-1904 [10.1089/ars.2006.8.1897].

Copper activates the NF-kappaB pathway in vivo

PERSICHINI, TIZIANA;PERCARIO, ZULEMA ANTONIA;COLASANTI, Marco;
2006-01-01

Abstract

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-kappaB 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-alpha (TNF-alpha), 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-kappaB activation. COX-2, a NF-kappaBdependent 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-kappaB.
Persichini, T., Percario, Z.A., Mazzon, E., Colasanti, M., Cuzzocrea, S., Musci, G. (2006). Copper activates the NF-kappaB pathway in vivo. ANTIOXIDANTS & REDOX SIGNALING, 8, 1897-1904 [10.1089/ars.2006.8.1897].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11590/148480
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