Dec, 2000
Possible role of elevation of glutathione in the acquisition of enhanced proliferation of mouse splenocytes exposed to small-dose gamma-rays
International Journal of Radiation Biology
- ,
- ,
- ,
- Volume
- 76
- Number
- 12
- First page
- 1641
- Last page
- 1647
- Language
- English
- Publishing type
- Research paper (scientific journal)
- DOI
- 10.1080/09553000050201136
- Publisher
- TAYLOR & FRANCIS LTD
Purpose: To examine the relation between the induction of an increased glutathione level and the elevated proliferative response of mouse splenocytes by a small dose of gamma -rays.
Materials and methods: Male ICR strain mice, 7 weeks of age, were divided into irradiated and non-irradiated control groups. irradiation was done with gamma -rays from a Cs-137 source at a dose of 50 cGy (1.11 Gy/min). Glutathione content in the splenocytes was measured using a modified spectrophotometric technique. Concanavalin A (Con A)-induced proliferative response of the splenocytes after whole-body gamma -ray irradiation was estimated from the H-3-thymidine incorporation into the cells.
Results: The glutathione level in mouse splenocytes increased 2 h after whole-body gamma -ray irradiation at 50 cGy, peaked at 4-h and thereafter decreased almost to the zero-time level by 12-h postirradiation. A significant enhancement of Con A-induced proliferation was observed in the splenocytes obtained from the whole-body-irradiated animals between 2 h and 6 h post-irradiation. Glutathione exogenously added to splenocytes obtained from normal mice enhanced the Con A-induced proliferation of splenocytes in a dose-dependent manner. This enhancement was completely blocked by buthionine sulfoximine, a specific inhibitor of the de novo pathway of glutathione synthesis.
Conclusions: The induction of endogenous glutathione immediately after low-dose gamma -ray irradiation is at least partially responsible for the enhancement of immune function, and may throw light on the mechanisms of carcinostatic effects induced by low dose ionizing radiation.
Materials and methods: Male ICR strain mice, 7 weeks of age, were divided into irradiated and non-irradiated control groups. irradiation was done with gamma -rays from a Cs-137 source at a dose of 50 cGy (1.11 Gy/min). Glutathione content in the splenocytes was measured using a modified spectrophotometric technique. Concanavalin A (Con A)-induced proliferative response of the splenocytes after whole-body gamma -ray irradiation was estimated from the H-3-thymidine incorporation into the cells.
Results: The glutathione level in mouse splenocytes increased 2 h after whole-body gamma -ray irradiation at 50 cGy, peaked at 4-h and thereafter decreased almost to the zero-time level by 12-h postirradiation. A significant enhancement of Con A-induced proliferation was observed in the splenocytes obtained from the whole-body-irradiated animals between 2 h and 6 h post-irradiation. Glutathione exogenously added to splenocytes obtained from normal mice enhanced the Con A-induced proliferation of splenocytes in a dose-dependent manner. This enhancement was completely blocked by buthionine sulfoximine, a specific inhibitor of the de novo pathway of glutathione synthesis.
Conclusions: The induction of endogenous glutathione immediately after low-dose gamma -ray irradiation is at least partially responsible for the enhancement of immune function, and may throw light on the mechanisms of carcinostatic effects induced by low dose ionizing radiation.
- Link information
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- DOI
- https://doi.org/10.1080/09553000050201136
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/11133046
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000165906800008&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0033636192&origin=inward
- Scopus Citedby
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- ID information
-
- DOI : 10.1080/09553000050201136
- ISSN : 0955-3002
- Pubmed ID : 11133046
- SCOPUS ID : 0033636192
- Web of Science ID : WOS:000165906800008