| Increased rhodamine 123 uptake by carcinoma cells. | |
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MedLine Citation:
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PMID: 4063967 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The total cellular content of the fluorescent mitochondrial-specific dye rhodamine 123 (Rh-123) was quantified by butanol extraction as a function of time of exposure and dose for a variety of cell lines. These results were compared with observations made by fluorescence microscopy on dye localization and mitochondrial morphology. There appeared to be two categories of cell types based on Rh-123 uptake: those which progressively accumulate the dye, such as Ehrlich ascites tumor cells, carcinoma-derived lines MCF-7, PaCa-2, EJ, HeLa, and normal fibroblast line CCL 64; and those which appear to equilibrate with the extracellular dye within 1 h of incubation in Rh-123 (1 microgram/ml) with a minimal level of uptake, such as the normal epithelial-derived lines CV-1 and MDCK and the transformed fibroblast line 64F3. Within the first category, the absolute value of uptake per cell correlated with the concentration of Rh-123 in the medium and with the period of exposure to the dye up to a point of apparent cellular saturation. The length of time required for apparent saturation depended on the cell type. In the second category equilibration was very early, and the total uptake was a function of the extracellular concentration of Rh-123. This probably does not represent a saturation level of dye content in the non-accumulating, low uptake cell lines. Fluorescence microscopy revealed that Rh-123 localization was initially mitochondrial-specific for all of the cell lines examined. Over time, alterations in mitochondrial morphology and cytoplasmic fluorescence were observed in the high uptake cell lines but not in the minimal uptake cell lines. Incubation of the high uptake HeLa cell line with the mitochondrial membrane potential inhibitor p-trifluoromethoxyphenylhydrazone substantially decreased Rh-123 uptake. These observations may indicate a transformation-related characteristic of carcinoma cell mitochondria. It may be possible to exploit the mechanism responsible for the progressive accumulation of Rh-123 by carcinoma-derived cell types for chemotherapeutic approaches to certain types of carcinomas. |
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Authors:
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K K Nadakavukaren; J J Nadakavukaren; L B Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Cancer research Volume: 45 ISSN: 0008-5472 ISO Abbreviation: Cancer Res. Publication Date: 1985 Dec |
Date Detail:
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Created Date: 1985-12-30 Completed Date: 1985-12-30 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2984705R Medline TA: Cancer Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 6093-9 Citation Subset: IM |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biological Transport / drug effects Butanols / diagnostic use Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology Carcinoma / metabolism* Cell Compartmentation / drug effects Cell Line Dose-Response Relationship, Drug Humans Membrane Potentials / drug effects Mitochondria / drug effects, metabolism* Rhodamine 123 Rhodamines / metabolism* Xanthenes / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Butanols; 0/Rhodamines; 0/Xanthenes; 370-86-5/Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; 62669-70-9/Rhodamine 123 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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