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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / metabolism
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Antineoplastic Agents / pharmacology*
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Apoptosis / drug effects*
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Caspase 3 / metabolism
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Caspase 9 / metabolism
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Cell Proliferation / drug effects
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Dequalinium / pharmacology*
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Humans
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K562 Cells / drug effects
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Leukemia / metabolism
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Leukemia / pathology*
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Membrane Potentials / drug effects
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Mitochondria / drug effects*
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Mitochondria / metabolism
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Mitochondrial Membranes / metabolism
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Oxygen / metabolism
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Reactive Oxygen Species / metabolism*
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Superoxides / metabolism*
Substances
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Antineoplastic Agents
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Reactive Oxygen Species
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Superoxides
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Adenosine Triphosphate
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Dequalinium
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Caspase 3
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Caspase 9
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Oxygen