Barros L F
Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad de Chile, Santiago.
Am J Obstet Gynecol. 1994 Jul;171(1):111-7. doi: 10.1016/s0002-9378(94)70086-9.
The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine.
Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast.
In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant approximately 90 mumol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 mumol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 +/- 45 mumol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected.
At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.
本研究旨在阐明胎盘清除次黄嘌呤所涉及的机制。
在原位灌注的豚鼠胎盘以及从人合体滋养层分离出的膜囊泡中测量同位素标记化合物的摄取情况。
在豚鼠中，次黄嘌呤摄取（从胎儿循环）通过一种可饱和的（米氏常数约为90 μmol/L）、依赖钠的机制进行，该机制被19 mmol/L罂粟碱抑制，但不被10 μmol/L硝基苄硫基肌苷或10 mmol/L尿苷抑制。尿苷摄取被硝基苄硫基肌苷阻断，但不被罂粟碱或4 mmol/L次黄嘌呤阻断。在人刷状缘（面向母体）膜囊泡中，次黄嘌呤内流不依赖钠，最适合用一个可饱和成分（米氏常数290±45 μmol/L）加一个线性成分来拟合。可饱和内流被罂粟碱阻断，但不被硝基苄硫基肌苷阻断。4 mmol/L次黄嘌呤不影响尿苷摄取。未检测到人基底（面向胎儿）膜囊泡介导的次黄嘌呤摄取。
在胎盘的血液 - 组织两个界面处，次黄嘌呤的转运都通过与核苷转运体不同的特定机制进行。
