Abstract
A recurrent problem in understanding the pathophysiology of the fetal alcohol syndrome (FAS) is separation of the effects of alcohol drinking habits from other social habits (e.g. smoking). Work in this laboratory has suggested that in vivo ethanol (EtOH) and in vitro AcH inhibit A-A transport across the placenta, thereby contributing to the etiology of the FAS. Furthermore, it is known that pharmacologic concentrations of Nic inhibit A-A uptake by human placental villi. Therefore, we investigated the effect of physiologic concentrations of EtOH, AcH and Nic upon in vitro uptake of 14C-α-amino isobutyric acid (AIB) by human placental villi. In 4 experiments with EtOH (200 mg/dl) and Nic (0.2 uM), there was no difference (p > 0.2) (matched pair analysis) in 90 minute uptake of AIB between control (C) and EtOH, Nic or EtOH plus Nic exposed tissue. In 8 additional experiments, there was no difference (p > 0.2) between C and Nic (0.2 uM). AcH (2.0 uM) showed a trend for lowered uptake (% inhibition 11.1 ± 3.7, mean ± SEM) (p < 0.1). However, AcH plus Nic resulted in a significant (p < 0.03) reduction in AIB uptake (% inhibition 22.8 ± 4.9) when compared to C or AcH alone. CONCLUSION: (1) Nic alone, at a concentration found in smokers' sera, does not impair placental uptake of A-A. (2) AcH, at the very low concentration of 2.0 uM, causes slight inhibition of uptake. (3) Nic plus AcH appear to be synergistic, significantly inhibiting placental A-A uptake. Therefore, we speculate that cigarette smoking may potentiate placental insufficiency associated with EtOH ingestion.
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Fisher, S., Atkinson, M., Holzman, I. et al. 1120 IN VITRO INHIBITION OF HUMAN PLACENTAL AMINO ACID (A-A) UPTAKE: SYNERGISM BETWEEN NICOTINE (Nic) AND ACETALDEHYDE (AcH). Pediatr Res 15 (Suppl 4), 629 (1981). https://doi.org/10.1203/00006450-198104001-01146
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DOI: https://doi.org/10.1203/00006450-198104001-01146