Resistance to Tetracycline, a Hydrophilic Antibiotic, Is Mediated by P-Glycoprotein in Human Multidrug-Resistant Cells
Two multidrug-resistant human leukemic CCRF-CEM sublines (CEM/VCR R and CEM/VLB100) were significantly more resistant to tetracycline, a hydrophilic antibiotic, than parental cells (P < 0.001). Verapamil and cyclosporin A completely reversed tetracycline resistance in CEM/VCR R cells, which also...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1993-01, Vol.190 (1), p.79-85 |
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| creator | Kavallaris, M. Madafiglio, J. Norris, M.D. Haber, M. |
| description | Two multidrug-resistant human leukemic CCRF-CEM sublines (CEM/VCR R and CEM/VLB100) were significantly more resistant to tetracycline, a hydrophilic antibiotic, than parental cells (P < 0.001). Verapamil and cyclosporin A completely reversed tetracycline resistance in CEM/VCR R cells, which also accumulated and retained significantly less [3H]tetracycline than CCRF-CEM cells. Like verapamil, addition of tetracycline to CEM/VCR R cells which had achieved steady-state vincristine levels resulted in augmented vincristine accumulation. [3H]Azidopine photoaffinity labelling of CEM/VCR R membrane proteins was inhibited by tetracycline in a dose-dependent manner. Although drugs associated with the multidrug-resistance phenotype are typically hydrophobic compounds, these data suggest that resistance to tetracycline, despite its hydrophilic nature, is mediated by P-glycoprotein in these cell lines. |
| doi_str_mv | 10.1006/bbrc.1993.1013 |
| format | Article |
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Verapamil and cyclosporin A completely reversed tetracycline resistance in CEM/VCR R cells, which also accumulated and retained significantly less [3H]tetracycline than CCRF-CEM cells. Like verapamil, addition of tetracycline to CEM/VCR R cells which had achieved steady-state vincristine levels resulted in augmented vincristine accumulation. [3H]Azidopine photoaffinity labelling of CEM/VCR R membrane proteins was inhibited by tetracycline in a dose-dependent manner. Although drugs associated with the multidrug-resistance phenotype are typically hydrophobic compounds, these data suggest that resistance to tetracycline, despite its hydrophilic nature, is mediated by P-glycoprotein in these cell lines.</description><subject>ATP-Binding Cassette, Sub-Family B, Member 1</subject><subject>Biological Transport</subject><subject>CCRF-CEM cells</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cyclosporine - pharmacology</subject><subject>Drug Resistance - physiology</subject><subject>Humans</subject><subject>leukemia</subject><subject>man</subject><subject>mediation</subject><subject>Membrane Glycoproteins - physiology</subject><subject>multidrug resistance</subject><subject>P-glycoprotein</subject><subject>tetracycline</subject><subject>Tetracycline - metabolism</subject><subject>Tetracycline - pharmacology</subject><subject>Tetracycline Resistance - physiology</subject><subject>Tumor Cells, Cultured</subject><subject>Verapamil - pharmacology</subject><subject>Vincristine - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFr2zAUh8XoaNOs190GOvVUZ5IlK9KxhC4ptHSMDHoTkvy8aTh2KskB__eTSdpbKQiEeJ9-enofQl8pWVBCxHdrg1tQpVg-UvYJzShRpCgp4WdoRjJRlIo-X6DLGP8RQikX6hydS6KYEGSGDr8g-phM5wCnHm8hBeNG1_oObrDBm7EO_f6vb73Dt13y1vfJuxt8H_Ej1N4kqLEd8c9i3Y6u34c-ge9wXpthZzr8OLTJ12H4U7w-k_AK2jZ-QZ8b00a4Ou1z9PvH3Xa1KR6e1ver24fCcSZSIZUk0ja2rpaNpNWSKcNFKRop8jdEpRiHUhHeCN7YzEneAGOVXQpXgoWyZHN0fczNrb0MEJPe-ehyB6aDfoh6WVUV44p8CFLB5TS0DC6OoAt9jAEavQ9-Z8KoKdGTET0Z0ZMRPRnJF76dkge7g_oNPynIdXmsQ57DwUPQ0XnIPmofwCVd9_696P_XpJpp</recordid><startdate>19930115</startdate><enddate>19930115</enddate><creator>Kavallaris, M.</creator><creator>Madafiglio, J.</creator><creator>Norris, M.D.</creator><creator>Haber, M.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19930115</creationdate><title>Resistance to Tetracycline, a Hydrophilic Antibiotic, Is Mediated by P-Glycoprotein in Human Multidrug-Resistant Cells</title><author>Kavallaris, M. ; 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Verapamil and cyclosporin A completely reversed tetracycline resistance in CEM/VCR R cells, which also accumulated and retained significantly less [3H]tetracycline than CCRF-CEM cells. Like verapamil, addition of tetracycline to CEM/VCR R cells which had achieved steady-state vincristine levels resulted in augmented vincristine accumulation. [3H]Azidopine photoaffinity labelling of CEM/VCR R membrane proteins was inhibited by tetracycline in a dose-dependent manner. Although drugs associated with the multidrug-resistance phenotype are typically hydrophobic compounds, these data suggest that resistance to tetracycline, despite its hydrophilic nature, is mediated by P-glycoprotein in these cell lines.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>8093660</pmid><doi>10.1006/bbrc.1993.1013</doi><tpages>7</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 1993-01, Vol.190 (1), p.79-85 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | ATP-Binding Cassette, Sub-Family B, Member 1 Biological Transport CCRF-CEM cells Cell Membrane - drug effects Cell Membrane - metabolism Cell Survival - drug effects Cyclosporine - pharmacology Drug Resistance - physiology Humans leukemia man mediation Membrane Glycoproteins - physiology multidrug resistance P-glycoprotein tetracycline Tetracycline - metabolism Tetracycline - pharmacology Tetracycline Resistance - physiology Tumor Cells, Cultured Verapamil - pharmacology Vincristine - metabolism |
| title | Resistance to Tetracycline, a Hydrophilic Antibiotic, Is Mediated by P-Glycoprotein in Human Multidrug-Resistant Cells |
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