ROS-mediated cytotoxic effect of copper(II) hydrazone complexes against human glioma cells.

Abstract

2-Acetylpyridine acetylhydrazone (H2AcMe), 2-benzoylpyridine acetylhydrazone (H2BzMe) and complexes [Cu(H2AcMe)Cl2] (1) and [Cu(H2BzMe)Cl2] (2) were assayed for their cytotoxicity against wild type p53 U87 and mutant p53 T98 glioma cells, and against MRC-5 fibroblast cells. Compounds 1 and 2 proved to be more active than the corresponding hydrazones against U87, but not against T98 cells. Compound 1 induced higher levels of ROS than H2AcMe in both glioma cell lines. H2AcMe and 1 induced lower levels of ROS in MRC5 than in U87 cells. Compound 2 induced lower levels of ROS in MRC5 than in T98 cells. The cytotoxic effect of 1 in U87 cells could be related to its ability to provoke the release of ROS, suggesting that the cytotoxicity of 1 might be somehow p53 dependent.

• Authors: Angel A Recio Despaigne, Jeferson G Da Silva, Pryscila R da Costa, Raquel G Dos Santos, Heloisa Beraldo
• Journal: Molecules (Basel, Switzerland) (Molecules) Vol. 19 Issue 11 Pg. 17202-20 (Oct 27 2014) ISSN: 1420-3049 [Electronic] Switzerland
• PMID: 25350363 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Hydrazones
• Reactive Oxygen Species
• Tumor Suppressor Protein p53
• Copper

Topics

• Cell Line
• Cell Line, Tumor
• Copper (pharmacology)
• Fibroblasts (drug effects)
• Glioma (drug therapy, metabolism)
• Humans
• Hydrazones (pharmacology)
• Reactive Oxygen Species (metabolism)
• Tumor Suppressor Protein p53 (metabolism)