Abstract
Low dose radiation is known to induce anti-oxidative substances, which suppress DNA damages, and activate DNA repair system. Since human being are exposed to multiple environment carcinogens, the effect of radiation may result from the combined exposures with these factors. Little is known, however, if low dose radiation affects carcinogenic responses induced by the other carcinogens. In this study, we examined if the pre-exposure of low dose radiation may affect the mutation induction and T-cell lymphoma development in thymus after exposure to chemical carcinogen, N-ethyl-N-nitrosourea (ENU).
B6C3F1 or B6C3F1 (gpt-delta) mice were exposed to X-rays (0.2 or 1.0 Gy per week) for 4 consecutive weeks, and then treated with ENU (200 ppm) in drinking water. Lymphoma incidence and mutation frequency in thymus after the exposures were analyzed. The incidence of lymphomas by single treatment with ENU or X-rays was less than 20%. The incidence of ENU-induced lymphomas was reduced by pre-exposure of 0.2 Gy, in contrast that it was increased by pre-exposure of 1.0 Gy. The gpt-assay also revealed that pre-exposure of 0.2 Gy reduced the frequency of ENU-induced mutation, whereas pre-exposure of 1.0 Gy increased. Especially, the reduction of G to A base substitution and clonally expansion of mutant cells by pre-exposure of 0.2 Gy may contribute to the decrease of lymphoma incidence and mutant frequency. These results suggest that the low dose radiation work on chemical damage (s), showing crosstalk of radiation with chemical response.
This study was supported through a grant of LRI by JCIA.
