Effects of Ionizing Radiation and Cisplatin on Peroxiredoxin I & II Expression and Survival Rate in Human Neuroblastoma and Rat Fibroblast Cells.
- Author:
Sung Hwan KIM
1
;
Sei Chul YOON
Author Information
1. Department of Radiation Oncology, The Catholic University of Korea, Seoul, Korea. kimandre@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
PrxI;
PrxII;
Ionizing radiation;
Cisplatin;
Rat2 cell line;
SK-N-BE2C cell line
- MeSH:
Acetylcysteine;
Animals;
Antioxidants;
Blotting, Western;
Cell Line;
Cisplatin*;
Fibroblasts*;
Humans*;
Neuroblastoma*;
Peroxiredoxins*;
Radiation, Ionizing*;
Rats*;
Survival Rate*
- From:The Journal of the Korean Society for Therapeutic Radiology and Oncology
2006;24(4):272-279
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: This study investigated the influence of irradiation and cisplatin on PrxI & PrxII expression and on their survival rates (SR) in SK-N-BE2C and Rat2 cell lines. MATERIALS AND METHODS: The amount of PrxI & PrxII production with or without N-acetyl-L-cysteine (NAC) pretreatment was studied using a western blot after 20 Gy irradiation to determine the degree of inhibition of ROS accumulation. In addition, the amount of PrxI & PrxII production after cisplatin and after combination with cisplatin and 20 Gy irradiation was studied. The SRs of the cell lines in SK-N-BE2C and Rat 2 cells, applied with 20 Gy irradiation only, with various concentrations of cisplatin and with the combination of both, were studied. The 20 Gy irradiation-only group and the combination group were each subdivided according to NAC pretreatment, and corresponding SRs were observed at 2, 6, 12 and 48 hours after treatment. RESULTS: Compared with the control group, the amount of PrxI in SK-N-BE2C increased up to 60 minutes after irradiation and slightly increased after irradiation with NAC pretreatment 60 minutes. It did not increase in Rat2 after irradiation regardless of NAC pretreatment. PrxII in SK-N-BE2C and Rat2 was not increased after irradiation regardless of NAC pretreatment. The amounts of PrxI and PrxII in SK-N-BE2C and Rat2 were not increased either with the cisplatin-only treatment or the combination treatment with cisplatin and irradiation. SRs of irradiation group with or without NAC pretreatment and the combination group with or without NAC pretreatment were compared with each other in SK-N-BE2C and Rat2. SR was significantly high for the group with increased amount of PrxI, NAC pretreatment and lower the cisplatin concentration. SR of the group in SK-N-BE2C which had irradiation with NAC pretreatment tended to be slightly higher than the group who had irradiation without NAC pretreatment. SR of the group in Rat2 which had irradiation with NAC pretreatment was significantly higher than that the group which had irradiation without NAC pretreatment. Compared to the combination group, the irradiation-only group revealed statistically significant SR decrease with the maximal difference at 12 hours. However, at 48 hours the SR of the combination group was significantly lower than the irradiation-only group. CONCLUSION: PrxI is suggested to be an antioxidant enzyme because the amount of PrxI was increased by irradiation but decreased pretreatment NAC, a known antioxidants. Furthermore, cisplatin may inhibit PrxI production which may lead to increase cytotoxicity of irradiation. The expression of PrxI may play an important role in cytotoxicity mechanism caused by irradiation and cisplatin.
