Abstract
Depolarisation of the plasma membrane has been shown to be actively regulated during lymphocyte-apoptosis. Here, we present data about anti-Fas and As2O3 induced depolarisation of myeloid U-937 cells. Anti-Fas but not As2O3-induced depolarisation was significantly dependent on caspase-activation. Na+-fluxes contributed to the depolarisation in early stages of As2O3-induced apoptosis, whereas the membrane potential in late stages depended on Cl- -fluxes. Cl- -channels also played an important role in the induction of cell shrinkage in As2O3-induced apoptosis. However, none of these ions contributed significantly to anti-Fas induced depolarisation. This indicates the existence of different mechanisms for apoptotic plasma membrane depolarisation within one cell type.
MeSH terms
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4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology
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Antibodies, Monoclonal / metabolism
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Antibodies, Monoclonal, Murine-Derived
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Antineoplastic Agents / pharmacology*
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Apoptosis / physiology*
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Arsenic Trioxide
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Arsenicals / pharmacology*
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Cell Membrane / metabolism*
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Chloride Channels / metabolism
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Chlorides / metabolism
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Humans
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Membrane Potentials / drug effects
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Membrane Potentials / physiology*
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Myeloid Cells* / cytology
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Myeloid Cells* / drug effects
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Myeloid Cells* / physiology
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Nitrobenzoates / pharmacology
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Oxides / pharmacology*
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Sodium / metabolism
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U937 Cells
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fas Receptor / immunology
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fas Receptor / metabolism*
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Murine-Derived
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Antineoplastic Agents
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Arsenicals
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Chloride Channels
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Chlorides
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Nitrobenzoates
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Oxides
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anti-Fas monoclonal antibody
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fas Receptor
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5-nitro-2-(3-phenylpropylamino)benzoic acid
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Sodium
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4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid
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Arsenic Trioxide