The novel N-heterocyclic carbene ligand precursor NaHImPrSO3 (sodium 3,3'-(1H-imidazole-3-ium-1,3-diyl)dipropane-1-sulfonate) and the related silver carbene complex [Na4(ImPrSO3)2]AgCl have been synthesized and characterized. Recrystallization of the analogous [ImAcEt]AgCl complex allowed the development of X-ray analysis which led to achieve relevant structural information concerning this silver(I) derivative. Both sulfonate- and ester-functionalized silver(I) N-heterocyclic carbenes (NHCs) were evaluated for their antiproliferative activities in a wide panel of human cancer cells. Complex [Na4(ImPrSO3)2]AgCl showed a significant in vitro antiproliferative activity that was correlated with its strong ability to inhibit thioredoxin reductase. The inhibition of this selenoenzyme determined an alteration of the cellular redox environment thus leading to the induction of the apoptotic cell death through the activation of the ASK-1 pathway.

Synthesis and in vitro antitumor activity of water soluble sulfonate- and ester-functionalized silver(I) N-heterocyclic carbene complexes

PELLEI, Maura;MARINELLI, MARIKA;SANTINI, Carlo
2013-01-01

Abstract

The novel N-heterocyclic carbene ligand precursor NaHImPrSO3 (sodium 3,3'-(1H-imidazole-3-ium-1,3-diyl)dipropane-1-sulfonate) and the related silver carbene complex [Na4(ImPrSO3)2]AgCl have been synthesized and characterized. Recrystallization of the analogous [ImAcEt]AgCl complex allowed the development of X-ray analysis which led to achieve relevant structural information concerning this silver(I) derivative. Both sulfonate- and ester-functionalized silver(I) N-heterocyclic carbenes (NHCs) were evaluated for their antiproliferative activities in a wide panel of human cancer cells. Complex [Na4(ImPrSO3)2]AgCl showed a significant in vitro antiproliferative activity that was correlated with its strong ability to inhibit thioredoxin reductase. The inhibition of this selenoenzyme determined an alteration of the cellular redox environment thus leading to the induction of the apoptotic cell death through the activation of the ASK-1 pathway.
2013
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/284181
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