A pulmonary origin of amniotic fluid thermolabile alkaline phosphatase near term

Abstract

Human alkaline phosphatase (EC 3.1.3.1 (AP)) isoenzymes are encoded by three different gene loci: intestinal, placental and various tissue non-specific isoforms [ 11. These last non-specific isoforms differ in their carbohydrate contents [2] and thermodenaturation behavior. Cytochemical and immunochemical procedures have shown the presence of a tissue non-specific AP isoform in normal lung type II cells [3,4]. This activity was related to the gestational age [3]. AP activity was also present in amniotic fluid: from the 30th week of gestation to term, AP activity (essentially thermolabile) increased in an exponential manner. This activity was linked to fetal lung maturity [5,6]. Both observations allow us to consider a possible role for the lung as the origin of AP activity in amniotic fluid during the final trimester of gestation. The aim of this work was, therefore, to examine this possible role with the help of ion exchange chromatography and electrophoretic separation of AP isoenzymes from fetal lung parenchyma and amniotic fluid.