Selenite-Induced Variation in Glutathione Peroxidase Activity of Three Mammalian Cell Lines: No Effect on Radiation-Induced Cell Killing or DNA Strand Breakage

The selenium-dependent glutathione peroxidase activities of three mammalian cell lines, HT29, P31, and N-18, cultured in medium with low serum content, increased about 2-, 5-, and 40-fold, respectively, after supplementation with 100 nM selenite. Catalase, CuZn superoxide dismutase, and Mn superoxid...

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Bibliographic Details
Published in:Radiation research 1989-02, Vol.117 (2), p.318-325
Main Authors: Sandström, Björn E., Carlsson, Jörgen, Marklund, Stefan L.
Format: Article
Language:English
Subjects:
Animals
Cell culture techniques
Cell Line
Cell lines
Cell Survival - drug effects
Cell Survival - radiation effects
Cultured cells
DNA
DNA Damage
DNA, Neoplasm - drug effects
DNA, Neoplasm - radiation effects
Glutathione Peroxidase - metabolism
HT29 cells
Humans
Irradiation
Mice
Radiation Tolerance
Selenious Acid
Selenium
Selenium - pharmacology
Space life sciences
Superoxides
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Summary:The selenium-dependent glutathione peroxidase activities of three mammalian cell lines, HT29, P31, and N-18, cultured in medium with low serum content, increased about 2-, 5-, and 40-fold, respectively, after supplementation with 100 nM selenite. Catalase, CuZn superoxide dismutase, and Mn superoxide dismutase activities were not generally influenced by selenite supplementation, and there was only a minor nonselenium-dependent glutathione peroxidase activity in the investigated cell lines. Gamma-irradiated control and selenite-supplemented cells showed no changes in the surviving fractions, as estimated by clonogenic survival or [3 H]-thymidine uptake, nor were there any significant differences between the two groups in the induction of DNA strand breaks after γ irradiation under repairing (37°C) or nonrepairing (0°C) conditions. The results suggest that selenium-dependent glutathione peroxidase does not contribute significantly to the radiation resistance of cultured mammalian cells.
ISSN:0033-7587
1938-5404
DOI:10.2307/3577332