HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 72/3/628    most recent biolreprod.104.032318v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal My Folders Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Miceli, F. Articles by Apa, R. Search for Related Content PubMed PubMed Citation Articles by Miceli, F. Articles by Apa, R. Agricola Articles by Miceli, F. Articles by Apa, R.

Effects of Nicotine on Human Luteal Cells In Vitro: A Possible Role on Reproductive Outcome for Smoking Women¹

Cattedra Di Fisiopatologia Della Riproduzione Umana,³ Università Cattolica Del Sacro Cuore, 00168 Roma, Italy Istituto Scientifico Internazionale (ISI) "Paolo VI,"⁴ Università Cattolica Del Sacro Cuore, 00168 Roma, Italy OASI Institute For Research,⁵ 94018 Troina, Italy

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 PGF₂ release from luteal cells, with a dose-related efficacy for M-nicotine. On the contrary, PGE₂ 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.

¹ Supported by Italian Health Ministry. Current Research: 2003; "La prevenzione dell' handicap mentale: modelli di studio biologici e clinici in epoca preconcenzionale, riproduttiva e prenatale."

² Correspondence: Rosanna Apa, Cattedra Di Fisiopatologia Della Riproduzione Umana, Università Cattolica Del Sacro Cuore, Largo A. Gemelli 8, 00168 Roma, Italia. FAX: 39 06 3051160; krimisa{at}libero.it

This article has been cited by other articles:

				S. P. Ng, B. G. Steinetz, S. G. Lasano, and J. T. Zelikoff Hormonal Changes Accompanying Cigarette Smoke-Induced Preterm Births in a Mouse Model Experimental Biology and Medicine, September 1, 2006; 231(8): 1403 - 1409. [Abstract] [Full Text] [PDF]