Abstract
Biological sensitivity to radiation differs among cell and organ types, as well as their state of cell cycle when irradiated. This difference in radiation sensitivity can be attributed to multiple factors, including the amount or kind of DNA damage and mechanisms of damage response and repair.
The effect of DNA exposure to radiation is both direct and indirect. The direct effect is the physical break, single or double, in DNA following ionizing radiation exposure. Free radical species, a product of the interaction between radiation and cellular water, results in many chemical and biological changes, producing an indirect effect. Of the latter, prolonged oxidative stress caused by low LET radiation is a risk factor for the alteration of genetic information. Mutations in somatic cells can result in cancer and other diseases, while those occurred in germ cells could potentially be inherited to offspring, and lead to congenital disorders.
To study the effects of radiation-induced oxidative DNA damage and its repair mechanism, we analyzed the DNA damage response in the testis and intestine of X-ray irradiated mice, including damage status, degree of cell death and cell proliferation. Radiation exposure for 2 days and 7 days at 0.5, 1, 2, and 4Gy revealed a pattern of increased immunoreactivity in gH2AX, 53BP1 and Rad51, as well as a decrease in the number of BrdU positive cells within the testis. The same result was not observed in intestinal samples at those time points. The nuclear content of 8-oxoguanine, an oxidized form of guanine, was also analyzed together with the expression of repair factors in different cell types.
