INDUCTION AND REPAIR OF DNA DOUBLE-STRAND BREAKS IN MAMMALIAN CELLS CONTINUOUSLY EXPOSED TO gamma -RADLATION

• Published in: Health physics (1958) Vol. 105; no. 1; p. S24
• Main Authors: Anchishkina, NA, Smetanina, N M, Archangelskaya, E Y, Vorobyeva, N Y, Guryev, D V, Osipov, AN
• Format: Journal Article
• Language: English
• Published: 01-07-2013
• ISSN: 0017-9078

The aim of the present work was to study of the DNA double-strand break (DSB) formation in Chinese hamster cells (V79 line) depending on the dose rate and time of gamma -radiation exposure. The apoptotic cells' frequency and production of reactive oxygen species (ROS) were also evaluated. It was shown that the dose-response curve for the phosphorylated histone H2AX ( gamma -H2AX) foci (a well known marker of DNA DSB) formation in cells exposed to a high dose-rate (400 cGy min super(-1)) was described by a linear function of y = 1.22 + 23.11x, where "y" is the mean of the gamma -H2AX foci number in the cell nucleus and "x" is the radiation dose in Gy. Decreasing the dose rate to 10 mGy min super(-1) leads to a decrease in the gamma -H2AX foci formation and changes the shape of the dose-effect curve; i.e., a linear increase of the foci number up to a dose of 1.44 Gy and the "plateau" appearance in the dose range of 1.44-4.32 Gy. There was only a weak increase in the foci number in the cells irradiated with a low dose rate (1 mGy min super(-1)). The character of changes in the number of gamma -H2AX foci in cells irradiated with a very low dose-rate (0.1 mGy min super(-1)) is unusual; there was a slight increase of the foci number at the early stages of exposure time (6-24 h, doses 3.6-14.4 cGy), while increasing exposition time and, therefore, the radiation dose (48-72 h, 28.8-43.2 cGy) caused a decrease in the number of gamma -H2AX foci to almost the control level. There were no changes in the apoptotic cells' frequency after exposure at this dose-rate; however, the results of the ROS production measurements showed that changes in the ROS production rate are associated with the gamma -H2AX foci number in these cells. The effects observed at a very low dose-rate irradiation could be explained based on the suggested inducibility of the DNA repair or antioxidant systems once the threshold for signaling has been reached. These results provide further support for non-linearity in the biological effects of low dose radiation at a molecular level of DNA lesions.