Dequalinium induces cell death in human leukemia cells by early mitochondrial alterations which enhance ROS production.

Abstract

Dequalinium (DQA) has been proposed as a selective antitumoral agent due to its preferential accumulation in mitochondria of cancer cells. Our aim was a better understanding of DQA cytotoxicity. DQA-induced NB4 and K562 cell alterations are initiated within the first 30 min of treatment at a high DQA concentration with a mitochondrial membrane depolarization. Cytochrome c release to cytoplasm, superoxide anion overproduction and ATP depletion in NB4 cells induce, 16 h later, apoptosis by a typical caspase-9/caspase-3-dependent intrinsic pathway. K562 cells were more resistant to the DQA effect than NB4 cells, remaining viable for longer time periods.

• Authors: Pilar Sancho, Eva Galeano, Elena Nieto, M Dolores Delgado, Ana Isabel García-Pérez
• Journal: Leukemia research (Leuk Res) Vol. 31 Issue 7 Pg. 969-78 (Jul 2007) ISSN: 0145-2126 [Print] England
• PMID: 17250890 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• Reactive Oxygen Species
• Superoxides
• Adenosine Triphosphate
• Dequalinium
• Caspase 3
• Caspase 9
• Oxygen

Topics

• Adenosine Triphosphate (metabolism)
• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Caspase 3 (metabolism)
• Caspase 9 (metabolism)
• Cell Proliferation (drug effects)
• Dequalinium (pharmacology)
• Humans
• K562 Cells (drug effects)
• Leukemia (metabolism, pathology)
• Membrane Potentials (drug effects)
• Mitochondria (drug effects, metabolism)
• Mitochondrial Membranes (metabolism)
• Oxygen (metabolism)
• Reactive Oxygen Species (metabolism)
• Superoxides (metabolism)