| 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
(Affiliation: Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Campus Universitario, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain.)
|
| Journal | Leukemia research
(Leuk Res)
Vol. 31
Issue 7
Pg. 969-78
(Jul 2007)
ISSN: 0145-2126 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
- Oxygen
- Caspase 3
- Caspase 9
|
| 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)
|
