Kalderon B, Dixon R M, Rajagopalan B, Angus P W, Oberhaensli R D, Collins J E, Leonard J V, Radda G K
Medical Research Council Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Oxford, United Kingdom.
Pediatr Res. 1992 Jul;32(1):39-44. doi: 10.1203/00006450-199207000-00008.
An oral load of 20 mg/kg galactose produces significant changes in the 31P magnetic resonance spectrum of the liver of a galactosemic patient. The peak at 5.2 ppm (which includes inorganic phosphate and galactose-1-phosphate) increased on two occasions to about twice its original size 60 min after galactose administration. An oral load of 10 mg/kg galactose given to a second patient produced no discernible changes at 30 min. We have also used an animal model of galactose intolerance, in which galactose metabolism in rats was blocked by the acute administration of ethanol. Studies in vivo and in vitro showed that the increase in the peak at 5.2 ppm was largely due to galactose-1-phosphate. We have shown in this preliminary study that small amounts of galactose can produce significant elevation of hepatic galactose-1-phosphate, which can be detected by 31P magnetic resonance spectroscopy.
给半乳糖血症患者口服20mg/kg的半乳糖会使其肝脏的31P磁共振波谱产生显著变化。5.2ppm处的峰(包括无机磷酸盐和1-磷酸半乳糖)在给予半乳糖60分钟后两次增加至约为原来大小的两倍。给第二位患者口服10mg/kg的半乳糖,30分钟时未产生可察觉的变化。我们还使用了半乳糖不耐受的动物模型,其中通过急性给予乙醇阻断大鼠体内的半乳糖代谢。体内和体外研究表明,5.2ppm处峰的增加主要归因于1-磷酸半乳糖。我们在这项初步研究中表明,少量半乳糖可使肝脏1-磷酸半乳糖显著升高,这可以通过31P磁共振波谱检测到。