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Metabolic Effects of Growth Factors and Polycyclic Aromatic Hydrocarbons on Cultured Human Placental Cells of Early and Late Gestation^*

Department of Pediatrics, McGill University-Montreal Children’s Hospital Research Institute, and Polypeptide Hormone Laboratory, McGill University Montreal, Quebec, Canada

Address requests for reprints to: Dr. Harvey Guyda, Division of Endocrinology and Metabolism, Montreal Children’s Hospital, 2300 Tupper Street, Room E-315, Montreal, Quebec, Canada H3H 1P3.

The metabolic effects of epidermal growth factor (EGF), insulin, insulin-like growth factor-I (IGF-I), and IGFII were determined on human placental cells in monolayer culture obtained from early gestation (<20 weeks) and late gestation (38–42 weeks). Parameters studied were uptake of aminoisobutyric acid (AIB), uptake of 3-O-methylglucose and [³H]thymidine incorporation into cell protein. Since benzo[] pyrene (BP) inhibits EGF binding and autophosphorylation in cultured human placental cells, particularly in early gestation, we also studied the effect of benzo[]pyrene and other polycyclic aromatic hydrocarbons (PAHs) on EGF-mediated AIB uptake.

The metabolic effects of EGF, insulin, and the IGFs in cultured human placental cells varied with gestational age and the growth factor studied. All three classes of growth factors stimulated AIB uptake in both early and late gestation at concentrations from 10–100 µg/L, well within a physiological range. However, insulin stimulation of AIB uptake was maximal at a high concentration (200 µg/L) in both early and late gestation cells, suggesting an action via type 1 IGF receptors rather than via insulin receptors. EGF stimulated 3-O-methylglucose uptake only in term placental cells. No significant stimulation of [³H]thymidine incorporation by any of the growth factors tested was seen with either early or late gestation cells.

The effect of PAHs on AIB uptake by cultured placental cells was variable. BP alone stimulated AIB uptake by both very early and late gestation cells and enhanced EGF-stimulated AIB uptake, -naphthoflavone alone inhibited AIB uptake at all gestational ages and inhibited EGF-stimulated AIB uptake. β-Naphthoflavone and 3-methylcholanthrene minimally inhibited AIB uptake by early gestation cells and did not modify EGFstimulated uptake at any gestational period.

Our prior results demonstrated that BP more significantly inhibited EGF than IGF or insulin receptor binding as well as autophosphorylation in early gestation placenta, and that BP was the most potent of the PAHs tested. Thus, the direct effect of the PAHs on placental EGF receptors and amino acid transport may indicate altered function of EGF in the regulation of placental growth in smoking mothers that is developmentally regulated.

^* This work was supported by Medical Research Council of Canada Grant MT-4403.

Received June 25, 1990.

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