Slavin S, Yatziv S
Science. 1980 Dec 5;210(4474):1150-2. doi: 10.1126/science.7003711.
Enzyme deficiency was corrected in mice after allogeneic bone marrow transplantation with occurrence of graft versus host disease. beta-Glucuronidase-deficient C3H/HeJ mice were treated with total lymphoid irradiation. Normal bone marrow cells (30 X 10(6)) from BALB/c to C3H/HeJ chimeras (>90 percent circulating donor-type cells) without graft versus host disease. beta-Glucuronidase activity increases to normal levels in all chimeras as measured in the liver and in the plasma. Activity was maintained throughout an observation period of 7 months.
在异基因骨髓移植后且出现移植物抗宿主病的小鼠中,酶缺乏得到了纠正。对β-葡萄糖醛酸酶缺陷的C3H/HeJ小鼠进行了全身淋巴照射。将来自BALB/c的正常骨髓细胞(30×10⁶)移植到C3H/HeJ嵌合体中(循环供体类型细胞>90%),未发生移植物抗宿主病。在肝脏和血浆中检测发现,所有嵌合体中的β-葡萄糖醛酸酶活性均升高至正常水平。在7个月的观察期内活性一直保持。