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Cellular glutathione is a key to the oxygen effect in radiation damage [1978](IR91)
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(Memo Item created on June 12, 2010 10:21 PM)- - - Begin title or keyword:
Cellular glutathione is a key to the oxygen effect in radiation damage
http://www.nature.com/nature/journal/v271/n5646/abs/271660a0.html
- - - End title or keyword:
Nature 271, 660 - 662 (16 February 1978); doi:10.1038/271660a0
Cellular glutathione is a key to the oxygen effect in radiation damage
M. L. MORSE & ROLF H. DAHL
Webb Waring Lung Institute, and Department of Biophysics and Genetics, University of Colorado Medical Center, Denver, Colorado 80262
OXYGEN is known to enhance biological changes induced by ionising radiation1,2. The changes include chromosome breaks (染色體斷裂) in Tradescantia 3 mutation ((基因的)突變, (生物物種的)突變) production in Drosophila, maize and bacteria3−6, and rate of mitosis ((【生】(細胞的)有絲分裂)) in grasshopper neuroblasts7. The biological and physical bases for the various enhancements remain obscure, and it has not yet been established that they are the result of a common mechanism. The quantitative aspects of the relationship between oxygen concentration and radiation response have been measured: for example, killing of Escherichia coli by X-ray radiation at a constant radiation dose8 and various interpretations of the quantitative aspects of the response base have been made9−12. Ionising radiation has been proposed to interact with water to produce several products and these products interact with cellular material to produce the biological effects observed. In the reactions proposed, cellular sulphydryl groups are supposed to be a primary cellular constituent which is reactive with the radiation products from water. We report here that one major cellular sulphydryl constituent, glutathione (GSH), is apparently the major component in the interaction between radiation products and the cell, for cells unable to synthesise glutathione cannot be protected against killing by ionising radiation by reduction of the external oxygen concentration.
References
1. Holthusen, H. Pflügers Archiv de gesante Physiologie 181, 1–25 (1921).
2. Kiefer, J. in Radiation Research: Biomedical, Chemical and Physical Perspectives, (ed. Nygaard, O. F.) 1025–1037 (Academic, New York, 1975).
3. Giles, N. H. & Riley, H. P. Proc. natn. Acad. Sci. U.S.A. 36, 336–344 (1950).
4. Baker, W. K. & Sgourakis, E. Proc. natn. Acad. Sci. U.S.A. 36, 176–184 (1950).
5. Schwartz, D. Proc. natn. Acad. Sci. U.S.A. 38, 490–494 (1952).
6. Hollaender, A., Baker, W. K. & Anderson, E. H. Cold Spring Harb. Symp. quant. Biol. 16, 315–326 (1951).
7. Gaulden, M. E. & Nix, M. Genetics 35, 665–666 (1950).
8. Hollaender, A. & Stapleton, G. E. Physiol. Rev. 33, 77–84 (1953).
9. Burnett, W. T., Stapleton, G. F., Morse, M. L. & Hollaender, A. Proc. Soc. exp. Biol. Med. 77, 636–638 (1951).
10. Burnett, W. T., Morse, M. L., Burke, A. W. & Hollaender, A. J. Bact. 63, 591–595 (1952).
11. Morse, M. L., Burke, A. W. & Burnett, W. T. J. Cell. comp. Physiol. 41, 407–417 (1953).
12. Alper, T. & Howard-Flanders, P. Nature 178, 978–979 (1956).
13. Fuchs, J. A. & Warner, H. R. J. Bact. 124, 140–148 (1975).
14. Apontoweil, P. & Berends, W. Biochim. biophys. Acta 399, 10–22 (1975).
15. Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. J. biol. Chcm. 193 265–275 (1951).
16. Bacq, Z. M. Experientia 7, 11–19 (1951).
17. Hollaender, A., Stapleton, G. E. & Burnett, W. T. in Use of Tracers in the Study of Biological Effects of Radiation 96–113 (CIBA Foundation, London, 1951).
18. Ashwood-Smith, M. J., Robinson, D. M., Barnes, J. H. & Bridges, B. A. Nature 216, 137–139 (1967).
19. Bridges, B. A. Adv. radiat. Biol. 3, 123–176 (1969).
20. Harris, J. W., Koch, C. J., Power, J. A. & Biaglow, J. E. Radiat. Res. 70, 585–596 (1977).
21. Bruce, A. K., Sansone, P. A. & MacVittie, T. J. Radiat. Res. 38, 95–108 (1969).
--------------------------------------------------------------------------------
© 1978 Nature Publishing Group
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// - - Begin memo item - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - //
(Memo Item created on June 12, 2010 10:21 PM)- - - Begin title or keyword:
Cellular glutathione is a key to the oxygen effect in radiation damage
http://www.nature.com/nature/journal/v271/n5646/abs/271660a0.html
- - - End title or keyword:
Nature 271, 660 - 662 (16 February 1978); doi:10.1038/271660a0
Cellular glutathione is a key to the oxygen effect in radiation damage
M. L. MORSE & ROLF H. DAHL
Webb Waring Lung Institute, and Department of Biophysics and Genetics, University of Colorado Medical Center, Denver, Colorado 80262
OXYGEN is known to enhance biological changes induced by ionising radiation1,2. The changes include chromosome breaks (染色體斷裂) in Tradescantia 3 mutation ((基因的)突變, (生物物種的)突變) production in Drosophila, maize and bacteria3−6, and rate of mitosis ((【生】(細胞的)有絲分裂)) in grasshopper neuroblasts7. The biological and physical bases for the various enhancements remain obscure, and it has not yet been established that they are the result of a common mechanism. The quantitative aspects of the relationship between oxygen concentration and radiation response have been measured: for example, killing of Escherichia coli by X-ray radiation at a constant radiation dose8 and various interpretations of the quantitative aspects of the response base have been made9−12. Ionising radiation has been proposed to interact with water to produce several products and these products interact with cellular material to produce the biological effects observed. In the reactions proposed, cellular sulphydryl groups are supposed to be a primary cellular constituent which is reactive with the radiation products from water. We report here that one major cellular sulphydryl constituent, glutathione (GSH), is apparently the major component in the interaction between radiation products and the cell, for cells unable to synthesise glutathione cannot be protected against killing by ionising radiation by reduction of the external oxygen concentration.
References
1. Holthusen, H. Pflügers Archiv de gesante Physiologie 181, 1–25 (1921).
2. Kiefer, J. in Radiation Research: Biomedical, Chemical and Physical Perspectives, (ed. Nygaard, O. F.) 1025–1037 (Academic, New York, 1975).
3. Giles, N. H. & Riley, H. P. Proc. natn. Acad. Sci. U.S.A. 36, 336–344 (1950).
4. Baker, W. K. & Sgourakis, E. Proc. natn. Acad. Sci. U.S.A. 36, 176–184 (1950).
5. Schwartz, D. Proc. natn. Acad. Sci. U.S.A. 38, 490–494 (1952).
6. Hollaender, A., Baker, W. K. & Anderson, E. H. Cold Spring Harb. Symp. quant. Biol. 16, 315–326 (1951).
7. Gaulden, M. E. & Nix, M. Genetics 35, 665–666 (1950).
8. Hollaender, A. & Stapleton, G. E. Physiol. Rev. 33, 77–84 (1953).
9. Burnett, W. T., Stapleton, G. F., Morse, M. L. & Hollaender, A. Proc. Soc. exp. Biol. Med. 77, 636–638 (1951).
10. Burnett, W. T., Morse, M. L., Burke, A. W. & Hollaender, A. J. Bact. 63, 591–595 (1952).
11. Morse, M. L., Burke, A. W. & Burnett, W. T. J. Cell. comp. Physiol. 41, 407–417 (1953).
12. Alper, T. & Howard-Flanders, P. Nature 178, 978–979 (1956).
13. Fuchs, J. A. & Warner, H. R. J. Bact. 124, 140–148 (1975).
14. Apontoweil, P. & Berends, W. Biochim. biophys. Acta 399, 10–22 (1975).
15. Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. J. biol. Chcm. 193 265–275 (1951).
16. Bacq, Z. M. Experientia 7, 11–19 (1951).
17. Hollaender, A., Stapleton, G. E. & Burnett, W. T. in Use of Tracers in the Study of Biological Effects of Radiation 96–113 (CIBA Foundation, London, 1951).
18. Ashwood-Smith, M. J., Robinson, D. M., Barnes, J. H. & Bridges, B. A. Nature 216, 137–139 (1967).
19. Bridges, B. A. Adv. radiat. Biol. 3, 123–176 (1969).
20. Harris, J. W., Koch, C. J., Power, J. A. & Biaglow, J. E. Radiat. Res. 70, 585–596 (1977).
21. Bruce, A. K., Sansone, P. A. & MacVittie, T. J. Radiat. Res. 38, 95–108 (1969).
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© 1978 Nature Publishing Group
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