Abstract |
The effects of a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and/or an anti-promoter antipain ( protease inhibitor) on spontaneous and ultraviolet-induced sister-chromatid exchanges (SCEs) and 6-thioguanine-resistant (6TGr) recessive mutations were examined in V79 Chinese hamster cells in culture. TPA and/or antipain neither significantly altered base-line and UV-induced immediate SCE frequencies, nor decreased the level of delayed SCEs which persisted 6-7 days after irradiation. TPA and/or antipain appeared to enhance the recovery of UV-induced 6TGr colonies at the plateau expression phase despite non-mutagenicity by themselves and unaltered metabolic cooperation. Thus, the results conceivably imply that the 6TGr-recessive mutation expression, but not fixation, can be modulated at the cell level by TPA and/or antipain. Our results, together with the recent results of Loveday and Latt, may argue against the notion that TPA enhances the antipain-suppressible SCEs as an index of mitotic recombination in relevance with a tumor-promotion mechanism.
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Authors | Y Fujiwara, Y Kano, M Tatsumi, P Paul |
Journal | Mutation research
(Mutat Res)
Vol. 71
Issue 2
Pg. 243-51
(Jul 1980)
ISSN: 0027-5107 [Print] Netherlands |
PMID | 7393240
(Publication Type: Journal Article)
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Chemical References |
- Oligopeptides
- Phorbols
- Antipain
- Thioguanine
- Tetradecanoylphorbol Acetate
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Topics |
- Animals
- Antipain
(pharmacology)
- Cell Line
- Cricetinae
- Cricetulus
- Crossing Over, Genetic
(drug effects)
- Mutation
- Oligopeptides
(pharmacology)
- Phorbols
(pharmacology)
- Sister Chromatid Exchange
(drug effects, radiation effects)
- Tetradecanoylphorbol Acetate
(pharmacology)
- Thioguanine
(pharmacology)
- Ultraviolet Rays
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