Human placental transfer of zinc: normal characteristics and role of ethanol.

Abstract

The fetal alcohol syndrome is primarily an impairment of growth and development. Zinc deficiency also causes abnormal fetal growth. Moreover, alcohol has been shown in some rodent studies to impair placental transport of zinc. The purpose of this investigation was to define better normal human placental zinc transport and the effects of alcohol on this process. To do this we employed the isolated perfused single cotyledon human term placental model, as well as the cultured human cytotrophoblast. In the perfused placental studies, it was shown that zinc is transferred by the placenta very slowly, about 6% of the rate of transport of antipyrine, a freely diffusible marker. The transfer is comparable in both directions, maternal to fetal and the reverse. Zinc does not cross the placenta against a zinc concentration gradient, in either direction. Rather there is good evidence of significant uptake (storage) of the zinc by the placenta on the recirculating compartment side of gradient studies. Moreover, when the perfusion fluid was low (0.2 g/100 ml) in albumin, about twice as much zinc accumulated in the perfused cotyledon and there was less zinc in the maternal compartment, as compared to perfusion with ten-fold higher (2.0 g/100 ml) albumin concentrations. Thus, ligand binding in the perfusate importantly influences placental zinc uptake. Interestingly, however, the increased placental binding of zinc did not translate into greater transfer of zinc to the fetal compartment. Thus, normal zinc transfer is slow, equal bidirectionally, and dependent on ligand binding in perfusate and placenta.(ABSTRACT TRUNCATED AT 250 WORDS)