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Wiley, Chemistry - A European Journal, 2(15), p. 314-318, 2008

DOI: 10.1002/chem.200801992

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Toxicity of copper(I)-NHC complexes against human tumor cells: induction of cell cycle arrest, apoptosis, and DNA cleavage.

Journal article published in 2008 by Marie-Laure Teyssot, Anne-Sophie Jarrousse, Aurélien Chevry, Angélique De Haze, Claude Beaudoin, Michèle Manin, Steven P. Nolan, Silvia Diez-Gonzalez, Laurent Morel, Arnaud Gautier
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Abstract

A copper(I)-NHC complex was compared with the metallodrug cisplatin, its cytotoxic and apoptotic properties were examined, and its effects on DNA were compared with other metal-NHC complexes differing in nature of the metal and the number of carbene ligands. The nature of cellular effects of the complex was also compared at the cell cycle and apoptotic levels by focusing on the breast tumor cell line MCF-7. The results indicate that exposing MCF-7 cells to the complex results in a dose-dependent production of protein kinase cdc2 (pcdc2). The passivity of the silver(I)- and palladium(II)-NHC complexes highlights the necessity of a copper(I) atom for nuclease activity and reinforces the hypothesis of a Fenton-type reaction. It is also seen that the complex arrests the cell cycle progression and induces apoptosis at a lower concentration.