Matalon R, Dorfman A
J Clin Invest. 1974 Oct;54(4):907-12. doi: 10.1172/JCI107830.
The Sanfilippo A syndrome is an autosomal recessive mucopolysaccharidosis characterized clinically by severe mental retardation and biochemically by storage in tissue and excretion in urine of excessive amounts of heparan sulfate. Since sulfamide groups are present in heparan sulfate, a sulfamidase deficiency could explain the impaired degradation of this polysaccharide. To investigate the enzymic basis of this disease, assays for sulfamidase were performed. Extracts of cultured fibroblasts and post-mortem liver were prepared by suspension of tissues in acetate: NaCl buffer, pH 4.5, containing Triton X-100 (Rohm and Haas Co., Philadelphia, Pa.), sonication, and centrifugation at 10,000 g. The supernatant fluid was incubated with [(35)S]-N-sulfated heparin. The release of inorganic sulfate after 18 h of incubation was determined by chromatography on Sephadex G-25. The liver and fibroblast extracts of patients with the Sanfilippo A syndrome showed a deficiency of sulfamidase. The quantity of heparan sulfate in fibroblasts derived from patients with Sanfilippo A, Hurler's and Hunter's diseases was found to be 7-10%, while it was about 1.25% of the total glycosaminoglycans in fibroblasts of normal controls.
Sanfilippo A综合征是一种常染色体隐性黏多糖贮积症,临床特征为严重智力发育迟缓,生化特征为组织中硫酸乙酰肝素蓄积及尿中大量排泄硫酸乙酰肝素。由于硫酸乙酰肝素中存在磺酰胺基团,磺酰胺酶缺乏可能解释了这种多糖降解受损的原因。为研究该疾病的酶学基础,进行了磺酰胺酶检测。培养的成纤维细胞提取物和尸检肝脏提取物的制备方法为:将组织悬浮于含Triton X - 100(罗姆哈斯公司,宾夕法尼亚州费城)的pH 4.5乙酸钠:氯化钠缓冲液中,超声处理,然后在10000g下离心。将上清液与[³⁵S]-N-硫酸化肝素一起孵育。孵育18小时后,通过在Sephadex G - 25上进行色谱分析来测定无机硫酸盐的释放量。Sanfilippo A综合征患者的肝脏和成纤维细胞提取物显示磺酰胺酶缺乏。发现Sanfilippo A、Hurler和Hunter病患者来源的成纤维细胞中硫酸乙酰肝素的量为7 - 10%,而正常对照成纤维细胞中硫酸乙酰肝素占总糖胺聚糖的量约为1.25%。