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

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.
AuthorsPilar Sancho, Eva Galeano, Elena Nieto, M Dolores Delgado, Ana Isabel García-Pérez
JournalLeukemia research (Leuk Res) Vol. 31 Issue 7 Pg. 969-78 (Jul 2007) ISSN: 0145-2126 [Print] England
PMID17250890 (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
  • 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)

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