Renlund M, Chester M A, Lundblad A, Parkkinen J, Krusius T
Eur J Biochem. 1983 Jan 17;130(1):39-45. doi: 10.1111/j.1432-1033.1983.tb07114.x.
Salla disease is a lysosomal storage disorder of unknown etiology, characterized biochemically by increased urinary excretion of N-acetylneuraminic acid. This compound has now been shown to occur in abnormally large amounts in liver and cultured skin fibroblasts from these patients. Quantification of N-acetylneuraminic acid was performed using a new gas-chromatography/mass spectrometric single-ion method which is sensitive and specific. No abnormalities in the activity of several enzymes involved in sialic acid metabolism (N-acetylneuraminate:pyruvate lyase, neuraminidase, CMP-N-acetylneuraminate N-acylneuraminohydrolase and CTP:N-acyl-neuraminate cytidylyltransferase) were demonstrable. A possible explanation for the defect is a malfunctioning active transport of N-acetylneuraminic acid across the lysosomal membrane.
萨勒病是一种病因不明的溶酶体贮积症,其生化特征是尿中N - 乙酰神经氨酸排泄增加。现已证明,这种化合物在这些患者的肝脏和培养的皮肤成纤维细胞中含量异常高。使用一种灵敏且特异的新型气相色谱/质谱单离子方法对N - 乙酰神经氨酸进行了定量分析。未发现参与唾液酸代谢的几种酶(N - 乙酰神经氨酸:丙酮酸裂解酶、神经氨酸酶、CMP - N - 乙酰神经氨酸N - 酰基神经氨酸水解酶和CTP:N - 酰基 - 神经氨酸胞苷酰转移酶)的活性有异常。该缺陷的一个可能解释是N - 乙酰神经氨酸跨溶酶体膜的主动转运功能失调。