Suzuki Y, Fukuoka K, Wey J J, Handa S
Clin Chim Acta. 1977 Feb 15;75(1):91-7. doi: 10.1016/0009-8981(77)90503-4.
beta-Galactosidase activities were studied in livers and leukocytes of mucopolysaccharidoses and mucolipidoses (I-cell disease and adult "beta-galactosidase deficiency" with macular cherry-red spots). Marked deficiency of hepatic 4-methylumbelliferyl (4MU) and GM1 beta-galactosidases was demonstrated in these diseases. Leukocyte GM1 beta-galactosidase was also deficient in mucolipidoses. The parents of the patients with I-cell disease and "beta-galactosidase deficiency" had normal beta-galactosidase activity in plasma and leukocytes, compared to the low enzyme activity in heterozygous carriers of GM1-gangliosidosis. The cause of this enzyme deficiency in these diseases is not clear at present. It seems to be affected seondarily by exgenous factors such as unknown stored materials in the cells. Mucopolysaccharides were not increased in the livers of two cases of I-cell disease and a case of "beta-galactosidase deficiency".
对黏多糖贮积症和黏脂贮积症(I型细胞病以及伴有黄斑樱桃红斑的成人“β-半乳糖苷酶缺乏症”)患者的肝脏和白细胞中的β-半乳糖苷酶活性进行了研究。在这些疾病中,肝脏4-甲基伞形酮(4MU)和GM1β-半乳糖苷酶明显缺乏。黏脂贮积症患者的白细胞GM1β-半乳糖苷酶也缺乏。与GM1神经节苷脂病杂合携带者中低酶活性相比,I型细胞病和“β-半乳糖苷酶缺乏症”患者的父母血浆和白细胞中的β-半乳糖苷酶活性正常。目前尚不清楚这些疾病中这种酶缺乏的原因。它似乎受到外源性因素如细胞中未知储存物质的继发影响。在两例I型细胞病和一例“β-半乳糖苷酶缺乏症”患者的肝脏中,黏多糖并未增加。