| First Author | Ogiu T | Year | 2000 |
| Journal | Radiat Res | Volume | 154 |
| Issue | 1 | Pages | 113-6 |
| PubMed ID | 10856972 | Mgi Jnum | J:63005 |
| Mgi Id | MGI:1860319 | Doi | 10.1667/0033-7587(2000)154[0113:aolbra]2.0.co;2 |
| Citation | Ogiu T, et al. (2000) Absence of linkage between radiosensitivity and the predisposing atp7b gene mutation for heritable hepatitis in the LEC rat. Radiat Res 154(1):113-6 |
| abstractText | The LEC rat is known to be a mutant strain that spontaneously develops heritable hepatitis due to copper accumulation, caused by mutation of the copper-transporting ATPase gene (Atp7b). Immunodeficiency and radiosensitivity have also been observed. Hayashi et al. extensively examined the radiosensitivity of the LEC rat and concluded that its hypersensitivity is controlled by a single autosomal gene. Furthermore, they suggested the possibility that it correlates to copper accumulation due to the Atp7b gene mutation, because ionizing radiation-induced hydroxyl radicals might act in concert with copper-induced hydroxyl radicals. In the present experiment, we analyzed linkage between radiosensitivity and the mutation responsible for hepatitis in F(1) animals of a cross with the F344 rat. Our results clearly demonstrated an absence of any significant association. In addition, partial dominance for radiosensitivity was observed, and radiosensitive (F(1) x LEC) backcross rats were twice as numerous as their radioresistant counterparts, suggesting the possibility of control by two or more recessive genes. |
