Daniels L B, Coyle P J, Glew R H, Radin N S, Labow R S
Arch Neurol. 1982 Sep;39(9):550-6. doi: 10.1001/archneur.1982.00510210020005.
Using glucocerebroside labeled with carbon 14 as the substrate, we determined that homogenates of brain tissue from both neuropathic and nonneuropathic cases of Gaucher's disease were profoundly deficient (more than 85%) in glucocerebrosidase activity. The beta-glucosidase activity, as measured with 4-methylumbelliferyl-beta-D-glucopyranoside as the substrate, in the homogenates of brain from four cases of Gaucher's disease was less sensitive to inhibition by conduritol B epoxide (CBE) when compared with normal brain beta-glucosidase. However, when homogenates were assayed with radiolabeled glucocerebroside as the substrate, no differential sensitivity toward CBE was indicated, suggesting the presence of an additional, CBE-insensitive, beta-glucosidase in brain tissue. Residual glucocerebrosidase activity partially purified from the brain of an adult with type 1 Gaucher's disease was activated threefold by gluconoyl hydrazine, whereas the same enzyme from control brain was unaffected, and eight times less sensitive to gluconolactone inhibition.
以碳-14标记的葡萄糖脑苷脂作为底物,我们测定出,戈谢病神经病变型和非神经病变型病例的脑组织匀浆中,葡萄糖脑苷脂酶活性严重缺乏(超过85%)。与正常脑β-葡萄糖苷酶相比,以4-甲基伞形酮基-β-D-吡喃葡萄糖苷作为底物测定的4例戈谢病患者脑匀浆中的β-葡萄糖苷酶活性,对环氧康杜立醇(CBE)抑制作用的敏感性较低。然而,当以放射性标记的葡萄糖脑苷脂作为底物对匀浆进行测定时,未显示出对CBE的差异敏感性,这表明脑组织中存在一种额外的、对CBE不敏感的β-葡萄糖苷酶。从一名成年1型戈谢病患者脑中部分纯化得到的残余葡萄糖脑苷脂酶活性,被葡糖酰肼激活了3倍,而来自对照脑的相同酶则未受影响,并且对葡糖内酯抑制作用的敏感性低8倍。