Abstract
We examined the relationship between the induction of glutathione (GSH) level in macrophage-like RAW264.7 cells by a low (adapting) dose γ-rays and the cell damage caused by a lethal dose of γ-rays at various intervals after the adapting dose. The reduced glutathione (GSH) level increased soon after exposure of the cells to 25 cGy of γ-rays, peaked between 3 hr and 6 hr, and returned almost to the zero time (0 hr) level by 24 hr post-irradiation. Cell damage was assessed by measuring the 3H-thymidine (3H-TdR) incorporation into cellular DNA. γ-Ray irradiation produced a dose-dependent cell damage in RAW cells, causing about 40% and 60% inhibition of 3H-TdR incorporation into DNA at 1.0 Gy and 2.0 Gy, respectively, as compared with non-irradiated cells. Treatment with the adapting dose of 25 cGy at 1 hr or 24 hr before the lethal irradiation was ineffective. However, pre-irradiation with 25 cGy at 3 hr or 6 hr prior to lethal irradiation inhibited the decrease of 3H-TdR incorporation into DNA, indicating a protective effect. GSH exogenously added to the medium also inhibited the cell damage induced by lethal doses of γ-Rays in a dose-dependent manner. These results indicate that the induction of endogenous GSH in living cells immediately following low-dose γ-Ray irradiation is at least partially responsible for the appearance of radioresistance to a subsequent lethal dose of radiation, and may make it possible to use higher doses of radiation in radiotherapy for tumor patients.
| Original language | English |
|---|---|
| Pages (from-to) | 5271-5275 |
| Number of pages | 5 |
| Journal | Anticancer Research |
| Volume | 19 |
| Issue number | 6 B |
| Publication status | Published - Nov 1999 |
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Keywords
- Glutathione
- Low-dose γ-ray
- Radioresistance
- RAW 264.7 cells
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Elevation of glutathione in RAW 264.7 cells by low-dose γ-ray irradiation and its responsibility for the appearance of radioresistance. / Kojima, Shuji; Matsumori, Shirane; Ono, Hideki; Yamaoka, Kiyonori.
In: Anticancer Research, Vol. 19, No. 6 B, 11.1999, p. 5271-5275.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Elevation of glutathione in RAW 264.7 cells by low-dose γ-ray irradiation and its responsibility for the appearance of radioresistance
AU - Kojima, Shuji
AU - Matsumori, Shirane
AU - Ono, Hideki
AU - Yamaoka, Kiyonori
PY - 1999/11
Y1 - 1999/11
N2 - We examined the relationship between the induction of glutathione (GSH) level in macrophage-like RAW264.7 cells by a low (adapting) dose γ-rays and the cell damage caused by a lethal dose of γ-rays at various intervals after the adapting dose. The reduced glutathione (GSH) level increased soon after exposure of the cells to 25 cGy of γ-rays, peaked between 3 hr and 6 hr, and returned almost to the zero time (0 hr) level by 24 hr post-irradiation. Cell damage was assessed by measuring the 3H-thymidine (3H-TdR) incorporation into cellular DNA. γ-Ray irradiation produced a dose-dependent cell damage in RAW cells, causing about 40% and 60% inhibition of 3H-TdR incorporation into DNA at 1.0 Gy and 2.0 Gy, respectively, as compared with non-irradiated cells. Treatment with the adapting dose of 25 cGy at 1 hr or 24 hr before the lethal irradiation was ineffective. However, pre-irradiation with 25 cGy at 3 hr or 6 hr prior to lethal irradiation inhibited the decrease of 3H-TdR incorporation into DNA, indicating a protective effect. GSH exogenously added to the medium also inhibited the cell damage induced by lethal doses of γ-Rays in a dose-dependent manner. These results indicate that the induction of endogenous GSH in living cells immediately following low-dose γ-Ray irradiation is at least partially responsible for the appearance of radioresistance to a subsequent lethal dose of radiation, and may make it possible to use higher doses of radiation in radiotherapy for tumor patients.
AB - We examined the relationship between the induction of glutathione (GSH) level in macrophage-like RAW264.7 cells by a low (adapting) dose γ-rays and the cell damage caused by a lethal dose of γ-rays at various intervals after the adapting dose. The reduced glutathione (GSH) level increased soon after exposure of the cells to 25 cGy of γ-rays, peaked between 3 hr and 6 hr, and returned almost to the zero time (0 hr) level by 24 hr post-irradiation. Cell damage was assessed by measuring the 3H-thymidine (3H-TdR) incorporation into cellular DNA. γ-Ray irradiation produced a dose-dependent cell damage in RAW cells, causing about 40% and 60% inhibition of 3H-TdR incorporation into DNA at 1.0 Gy and 2.0 Gy, respectively, as compared with non-irradiated cells. Treatment with the adapting dose of 25 cGy at 1 hr or 24 hr before the lethal irradiation was ineffective. However, pre-irradiation with 25 cGy at 3 hr or 6 hr prior to lethal irradiation inhibited the decrease of 3H-TdR incorporation into DNA, indicating a protective effect. GSH exogenously added to the medium also inhibited the cell damage induced by lethal doses of γ-Rays in a dose-dependent manner. These results indicate that the induction of endogenous GSH in living cells immediately following low-dose γ-Ray irradiation is at least partially responsible for the appearance of radioresistance to a subsequent lethal dose of radiation, and may make it possible to use higher doses of radiation in radiotherapy for tumor patients.
KW - Glutathione
KW - Low-dose γ-ray
KW - Radioresistance
KW - RAW 264.7 cells
UR - http://www.scopus.com/inward/record.url?scp=0033387454&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033387454&partnerID=8YFLogxK
M3 - Article
C2 - 10697548
AN - SCOPUS:0033387454
VL - 19
SP - 5271
EP - 5275
JO - Anticancer Research
JF - Anticancer Research
SN - 0250-7005
IS - 6 B
ER -