Radio-resistance induced by nitric oxide to heavy ion irradiation in A172 human glioma cells

LOW ENERGY ACCELERATOR, RAY TECHNOLOGY AND APPLICATIONS

Radio-resistance induced by nitric oxide to heavy ion irradiation in A172 human glioma cells

ZHOU Qingming，

ZHANG Hong，

ZHANG Xingxia

Nuclear Science and Techniques

Vol.18, No.5

pp.282-286

Published in print 20 Oct 2007

DOI：10.1016/S1001-8042(07)60062-1

CLC：Q691

43800

To investigate effects of nitric oxide on cellular radio-sensitivity, three human glioma cell lines, i.e. A172, A172 transfected green fluorescence protein (EGFP) gene (EA172) and A172 transfected inducible nitric oxide synthesis (iNOS) gene (iA172), were irradiated by ¹²C⁶⁺ ions to 0, 1 or 2Gy. Productions of nitric oxide and glutathione (GSH) in A172, EA172 and iA172 were determined by chemical methods, cell cycle was analyzed by flow cytometry at the 24th hour after irradiation, and survival fraction of the cells was measured by colorimetric MTT assay at the 5th day after irradiation. The results showed that the concentrations of nitric oxide and GSH in iA172 were significantly higher than in A172 and EA172; the G₂/M stage arrest induced by the ¹²C⁶⁺ ion irradiation was observed in A172 and EA172 but not in iA172 at the 24th hour after exposure; and the survival fraction of iA172 was higher than that of EA172 and iA172. Data suggest that the radio-sensitivity of the A172 was reduced after the iNOS gene transfection. The increase of GSH production and the change of cellular signals such as the cell cycle control induced by nitric oxide may be involved in this radio-resistance.

Nitric oxide12C 6+ heavy ionA172 human glioma cellsRadio-resistance

References

[1]

Worthington J, McCarthy H O, Barrett E, et al. J Gene Med, 2004, 6(6): 673-680.

[2]

Wang Z, Cook T, Alber S, et al. Cancer Res, 2004, 64: 1386-1395.

[3]

Mitchell J B, Wink D A, DeGraff W, et al. Cancer Res, 1993, 53: 5845-5848.

[4]

Matsumoto H, Hayashi S, Hatashita M, et al. Radiat Res, 2001, 155: 387-396.

[5]

Matsumoto H, Hayashi S, Hatashita M, et al. Int J Radiat Biol, 2000, 76: 1649-1657.

[6]

Matsumoto H, Hayashi S, Jin Z-H, et al. International Congress Series, 2002, 1236: 295-298.

[7]

May P, May E. Oncogene, 1999, 18: 7621-7636.

[8]

Taylor W R, DePrimo S E, Agarwal A, et al. Mol Biol Cell, 1999, 10: 3607-3622.

[9]

Zhu Q, Wani MA, El-Mahdy M, et al. J Biol Chem, 2000, 275: 11492-11497.

[10]

Hemish J, Nakaya N, Mittal V, et al. J Biol Chem, 2003, 278: 42321-42329.

[11]

Buckley B J, Whorton A R. Am J Physiol Cell Physiol, 2000, 279: C1168-1176.

[12]

Shanker G, Aschner M. Mol Brain Res, 2003, 110: 85-91.

[13]

Terato H, Ide H. Biol Sci Space, 2004, 18: 206-215.

[14]

Zhang M W, Peng X X, Hu P, et al. Acta Pharmacol Sin (in Chinese), 1998, 19: 121-127.

[15]

HUANG Qian, XU Ping, LIU Wenwen, et al. Chin J Ophthalmol (in Chinese), 2001, 37(4): 248-251.