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Reprod Toxicol. 2016 Oct;65:133-138. doi: 10.1016/j.reprotox.2016.06.014. Epub 2016 Jul 22.

Inhibition of placental 11beta-hydroxysteroid dehydrogenase type 2 by lead.

Author information

1
INRS-Institut Armand-Frappier, BioMed Research Center and Center for Interdisciplinary, Research on Well-Being, Health, Society and Environment (CINBIOSE), Laval, QC H7V 1B7, Canada.
2
INRS-Institut Armand-Frappier, BioMed Research Center and Center for Interdisciplinary, Research on Well-Being, Health, Society and Environment (CINBIOSE), Laval, QC H7V 1B7, Canada. Electronic address: cathy.vaillancourt@iaf.inrs.ca.

Abstract

Lead interferes with cortisol blood concentration, increases the risk of obstetrical complications, and could alter fetal development. The placenta controls maternal cortisol transfer to the fetus by the activity of the type 2 11β-hydroxysteroid dehydrogenase (11β-HSD2), which converts cortisol into inactive cortisone. This study determines the effect of lead on the expression and activity of the placental 11β-HSD2 in human trophoblast-like BeWo cells. Cells were treated with increasing concentration (0-1000nM) of PbCl2 for 24h. 11β-HSD2 protein expression was reduced by 45% at 1000nM of PbCl2 compared to untreated cells, while the activity was significantly reduced by PbCl2 at 10, 100 and 1000nM. This study shows the direct inhibitory action of lead on placental 11β-HSD2 activity and suggests that this heavy metal reduces the efficiency of the placental protection against the adverse effects of high cortisol level during fetal development.

KEYWORDS:

BeWo cell; Cortisol; Heavy metal; Human; Stress; Trophoblast

PMID:
27453427
DOI:
10.1016/j.reprotox.2016.06.014
[Indexed for MEDLINE]

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