INTRODUCTION

Although tobacco smoking is a widely recognized health hazard and a major cause of preventable mortality, consumption of tobacco remains a common practice in human societies. The association between smoking and various cancers, particularly lung disease, is well-known, but the effect of cigarette smoking on reproduction is still unclear. Several epidemiological studies have revealed a consistent and highly significant incidence of infertility as well as an increased risk of spontaneous abortion among smokers. Nevertheless, the mechanism of tobacco’s toxic effect on ovarian function remains unclear. canadian healthcare mall

Cigarette tobacco contains several substances. Carbohydrates and proteins are the most representative components, but alkaloids are significantly present as well. Nicotine, in particular, represents 90%-95% of total alkaloids. Nicotine is a highly toxic substance and is absorbed quickly through the respiratory tract, mouth mucosa, and skin. Approximately 80%-90% of nicotine is metabolized by the liver, but the kidneys and lungs are involved as well. Cotinine, one of the nicotine metabolites, has been detected in human ovarian follicular fluid and in granulosa-luteal cells. All this evidence indicates that nicotine can affect gamete cell functions.

In the present study, we investigated if nicotine and its methylated metabolite, A/-methyl-nicotine (M-nicotine), could affect progesterone production by human luteal cells. Because the cyclooxygenase pathway is strictly involved in the regulation of luteal steroidogenesis, we also looked for a possible influence of nicotine on the release of prostaglandins (PG). Finally, we tested the effect of nicotine and its metabolite on gene expression of vascular endothelial growth factor (VEGF), an angiogenic factor whose expression is directly correlated with a normal luteal function.