ArticleCurrent research in toxicology2022
The effect of ethanol and nicotine on ER stress in human placental villous explants.
Article in Current research in toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Placenta models for HIV-1-ART-nicotine comorbidity research: advances and remaining challenges.Cell death discovery · 2026Review
- Review
- Reactive oxygen species in fetal growth restriction mechanisms and therapeutic directions (Review).International journal of molecular medicine · 2026Review
- Current approaches and advances in placental toxicology.Trends in endocrinology and metabolism: TEM · 2026Review
- Dulaglutide and pregnancy: a comprehensive safety assessment using theFrontiers in pharmacology · 2025Article
- A stress paradox: the dual role of the unfolded protein response in the placenta.Frontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pregnant mothers continue smoking and drinking during pregnancy. To clarify the mechanisms of nicotine and ethanol toxicity during development, we have examined their effects on endoplasmic reticulum (ER) stress in human first trimester and term placental explants. First trimester and term human placental explants were treated with ethanol (2 ‰) or nicotine (15 µM), or their combination. The ER stress markers glucose regulated protein 78 (GRP78/BiP) and inositol requiring enzyme 1 α (IRE1α) were analyzed by immunoblotting. A statistically significant increase (p < 0.05) of GRP78/BiP by nicotine was noted in first trimester placental explants at 48 h, and in term placental explants at 24 h. Ethanol did not change protein expression of GRP78/BiP in either first trimester or term placental explants. IRE1α increased, although not statistically significantly, by all treatments in both first trimester and term placental explants. Thus, regardless of the known structural and functional differences in early and late placenta, both responded very similarly to the toxic compounds studied. These data support our earlier results in BeWo cells (Repo et al., 2014) implicating that nicotine induces ER stress in human placenta and may interfere with placental functions potentially disrupting fetal growth and development.
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Registered trials
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