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The carboxylic ionophore monensin inhibits active drug efflux and modulates in vitro resistance in daunorubicin resistant Ehrlich ascites tumor cells

Identifieur interne : 003233 ( Main/Exploration ); précédent : 003232; suivant : 003234

The carboxylic ionophore monensin inhibits active drug efflux and modulates in vitro resistance in daunorubicin resistant Ehrlich ascites tumor cells

Auteurs : Maxwell Sehested [Danemark] ; Torben Skovsgaard [Danemark] ; Henrik Roed [Danemark]

Source :

Biochemical Pharmacology [ 0006-2952 ] ; 1988.

RBID : ISTEX:7D4986BB327BDF545E06F64E134FD98A332E92F2

English descriptors

KwdEn :
- DNR, daunorubicin, EHR2, wild-type Ehrlich ascites tumor cell, EHR2/DNR+, daunorubicin resistant Ehrlich ascites tumor cell.
Teeft :
- Acidic, Ascites, Carboxylic, Carboxylic ionophores monensin, Cell suspensions, Daunorubicin, Drug efflux, Efflux, Ehr2, Ehrlich, Ehrlich ascites tumor cells, Exogenous amines, Glucose, Intracellular, Ionophores, Monensin, Nigericin, Phenotype, Pleiotropic, Pleiotropic resistance, Pleiotropic resistance phenotype, Present study, Resistant cells, Resistant subline, Skovsgaard, Sodium azide, Standard medium.

Abstract

Abstract: Acquired cellular resistance to anthracycline and vinca alkaloid drugs (pleiotroplc resistance) is commonly associated with reduced drug accumulation, a phenomenon which is thought to be partly due to increased energy-dependent drug efflux. We have previously detected increased plasma membrane traffic to, and content of, the acid endosomal compartment in pleiotroplc resistant Ehrlich ascites and P388 leukemia cells. This suggested that the endosome could be associated with the pleiotropic resistance phenotype by a mechanism of vesicular drug trapping and transport. The present study was undertaken in order to test the effects of the carboxylic ionophores monensin and nigericin, which are known to both disrupt intracellular vesicular traffic and to raise intravesicular pH, with relation to the pleiotropic resistance phenotype.Both monensin and nigericin increased daunorubicin (DNR) accumulation in daunorubicin resistant Ehrlich ascites tumor cells (EHR2/DNR+) in a dose-dependent manner. Further, monensin inhibited glucose induced DNR efflux from EHR2/DNR+ cells loaded with drug by energy deprivation. On the other hand, monensin had only negligible effect on DNR accumulation and efflux in wild-type Ehrlich ascites tumor cells (EHR2). In a clonogenic assay system, monensin reduced resistance to DNR in EHR2/DNR+, whereas only an additive effect was obtained in EHR2. However, both ionophores proved too toxic in in vivo experiments.These results, showing that drugs known to disrupt endosomal functions also inhibit the pleiotropic resistance phenotype, support the suggested link between the endosome and pleiotropic resistance.

Url:

https://api.istex.fr/ark:/67375/6H6-CJWH4X3B-6/fulltext.pdf

DOI: 10.1016/0006-2952(88)90643-0

Affiliations:

Danemark

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Abstract: Acquired cellular resistance to anthracycline and vinca alkaloid drugs (pleiotroplc resistance) is commonly associated with reduced drug accumulation, a phenomenon which is thought to be partly due to increased energy-dependent drug efflux. We have previously detected increased plasma membrane traffic to, and content of, the acid endosomal compartment in pleiotroplc resistant Ehrlich ascites and P388 leukemia cells. This suggested that the endosome could be associated with the pleiotropic resistance phenotype by a mechanism of vesicular drug trapping and transport. The present study was undertaken in order to test the effects of the carboxylic ionophores monensin and nigericin, which are known to both disrupt intracellular vesicular traffic and to raise intravesicular pH, with relation to the pleiotropic resistance phenotype.Both monensin and nigericin increased daunorubicin (DNR) accumulation in daunorubicin resistant Ehrlich ascites tumor cells (EHR2/DNR+) in a dose-dependent manner. Further, monensin inhibited glucose induced DNR efflux from EHR2/DNR+ cells loaded with drug by energy deprivation. On the other hand, monensin had only negligible effect on DNR accumulation and efflux in wild-type Ehrlich ascites tumor cells (EHR2). In a clonogenic assay system, monensin reduced resistance to DNR in EHR2/DNR+, whereas only an additive effect was obtained in EHR2. However, both ionophores proved too toxic in in vivo experiments.These results, showing that drugs known to disrupt endosomal functions also inhibit the pleiotropic resistance phenotype, support the suggested link between the endosome and pleiotropic resistance.</div>
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The carboxylic ionophore monensin inhibits active drug efflux and modulates in vitro resistance in daunorubicin resistant Ehrlich ascites tumor cells

The carboxylic ionophore monensin inhibits active drug efflux and modulates in vitro resistance in daunorubicin resistant Ehrlich ascites tumor cells

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri