Effects of Nicotine on Human Luteal Cells In Vitro: A Possible Role on Reproductive Outcome for Smoking Women

We investigated the effect of nicotine and its methylated metabolite, N -methyl-nicotine (M-nicotine), on human luteal cells by measuring release of progesterone and prostaglandins (PGs) from cultured cells and by testing gene expression of vascular endothelial growth factor (VEGF), an angiogenic fa...

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Bibliographic Details
Published in:Biology of reproduction 2005-03, Vol.72 (3), p.628-632
Main Authors: MICELI, Fiorella, MINICI, Francesca, LANZONE, Antonio, APA, Rosanna, TROPEA, Anna, CATINO, Stefania, ORLANDO, Mariateresa, LAMANNA, Giuseppina, SAGNELLA, Francesca, TIBERI, Federica, BOMPIANI, Adriano, MANCUSO, Salvatore
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
Dose-Response Relationship, Drug
Embryology: invertebrates and vertebrates. Teratology
Female
Fetal membranes
Fundamental and applied biological sciences. Psychology
General aspects. Development. Fetal membranes
Humans
In Vitro Techniques
Luteal Cells - drug effects
Luteal Cells - metabolism
Luteal Cells - secretion
Medical sciences
Nicotine - analogs & derivatives
Nicotine - metabolism
Nicotine - pharmacology
Nicotine - toxicity
Nicotinic Agonists - toxicity
Progesterone - metabolism
Progesterone - secretion
Prostaglandins - metabolism
Prostaglandins - secretion
Reproduction - drug effects
RNA, Messenger - analysis
Smoking - metabolism
Tobacco, tobacco smoking
Toxicology
Vascular Endothelial Growth Factor A - genetics
Vascular Endothelial Growth Factor A - metabolism
Vertebrates: reproduction
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Summary:We investigated the effect of nicotine and its methylated metabolite, N -methyl-nicotine (M-nicotine), on human luteal cells by measuring release of progesterone and prostaglandins (PGs) from cultured cells and by testing gene expression of vascular endothelial growth factor (VEGF), an angiogenic factor strictly involved in luteal pathophysiology. Primary cultures of human luteal cells were treated for 24 h with nicotine and M-nicotine (from 10 −6 to 10 −11 M) either alone or combined with hCG (25 ng/ml); progesterone and PGs were assayed in the culture medium. In another group of experiments, luteal cells were treated for 24 h with nicotine and M-nicotine (10 −7 M) to perform reverse transcriptase-polymerase chain reaction on VEGF mRNA. Nicotine and M-nicotine negatively affected basal luteal steroidogenesis at all tested concentrations, but neither was able to affect hCG-induced progesterone release. Both substances were able to significantly increase PGF 2α release from luteal cells, with a dose-related efficacy for M-nicotine. On the contrary, PGE 2 release was significantly inhibited by both nicotine and its metabolite. Finally, nicotine was able to increase VEGF mRNA expression significantly, whereas M-nicotine was not. In conclusion, nicotine and M-nicotine can induce a sort of luteal insufficiency by inhibiting progesterone release, probably through modulation of the PG system. Abstract Nicotine effects on steroidogenesis in human luteal cells are probably mediated by modulation of the prostaglandin system
ISSN:0006-3363
1529-7268
DOI:10.1095/biolreprod.104.032318