| Effects of selected anti-tumor-promoting chemicals on metabolic cooperation between Chinese hamster V79 cells. | |
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MedLine Citation:
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PMID: 7516098 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Many tumor-promoting chemicals inhibit gap junctional communication between cells. We investigated the possibility that antipromoting chemicals may act inversely and enhance gap junctional communication. The V79/metabolic cooperation assay is an in vitro test that measures gap junctional communication indirectly by determining the extent of metabolic cooperation between mutant and wild-type V79 Chinese hamster lung fibroblasts in culture. Six in vivo antipromoters (caffeine, 3-isobutyl-1-methylxanthine (IBMX), phenidone, dibromoacetophenone, tosylphenylalanine chloromethyl ketone (TPCK), and acetic acid) were tested in this assay to assess their effects on metabolic cooperation. Caffeine, IBMX, phenidone, and dibromoacetophenone had no effect on metabolic cooperation, while TPCK slightly inhibited metabolic cooperation in one V79 assay. Acetic acid appeared to facilitate metabolic cooperation. In tests where an antipromoter was combined with the established tumor promoter phorbol 12-myristate 13-acetate (PMA), acetic acid, caffeine, and IBMX counteracted PMA-induced inhibition of metabolic cooperation, while phenidone, dibromoacetophenone, and TPCK had little effect. These results indicate that some antipromoters interfere with the ability of a tumor-promoting chemical to inhibit metabolic cooperation and suggest that alteration of gap junctional communication can be a mechanism of antipromoter action. |
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Authors:
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L J Mills; S M Nelson; A R Malcolm |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: Toxicology and applied pharmacology Volume: 126 ISSN: 0041-008X ISO Abbreviation: Toxicol. Appl. Pharmacol. Publication Date: 1994 Jun |
Date Detail:
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Created Date: 1994-07-12 Completed Date: 1994-07-12 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0416575 Medline TA: Toxicol Appl Pharmacol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 338-44 Citation Subset: IM |
Affiliation:
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Science Applications International Corporation, U.S. Environmental Protection Agency, Narragansett, Rhode Island 02882. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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1-Methyl-3-isobutylxanthine
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pharmacology Acetic Acid Acetic Acids / pharmacology Acetophenones / pharmacology Animals Anticarcinogenic Agents / pharmacology* Arachidonic Acid / metabolism Caffeine / pharmacology Cell Communication / drug effects* Cells, Cultured Cricetinae Cricetulus Gap Junctions / drug effects* Lipoxygenase Inhibitors / pharmacology Mutation / drug effects Phosphodiesterase Inhibitors / pharmacology Phospholipases A / antagonists & inhibitors Protease Inhibitors / pharmacology Pyrazoles / pharmacology Tosylphenylalanyl Chloromethyl Ketone / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Acetic Acids; 0/Acetophenones; 0/Anticarcinogenic Agents; 0/Lipoxygenase Inhibitors; 0/Phosphodiesterase Inhibitors; 0/Protease Inhibitors; 0/Pyrazoles; 28822-58-4/1-Methyl-3-isobutylxanthine; 402-71-1/Tosylphenylalanyl Chloromethyl Ketone; 506-32-1/Arachidonic Acid; 58-08-2/Caffeine; 64-19-7/Acetic Acid; 92-43-3/phenidone; 99-73-0/4-bromophenacyl bromide; EC 3.1.1.-/Phospholipases A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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