Differences in sex hormone levels in the menstrual cycle due to tobacco smoking - myth or reality?

INTRODUCTION: Tobacco smoke contains, among others, polycyclic aromatic hydrocarbons (PAHs), heterocyclic analogues, aromatic amines, N-nitrosamines, volatile hydrocarbons, aldehydes, phenols, miscellaneous organic compounds, metals, and inorganic compounds. Tobacco smoking can harm women's reproductive system and may reduce fertility. The objective of the study was to explore the effect of tobacco smoke on the menstrual cycle due to smoking and second-hand smoke-exposure. MATERIAL AND METHODS: The study was performed on 153 women of reproductive age, who received care at the Gynaecological-Obstetric Clinical Hospital of the Poznan University of Medical Sciences. They were divided into three treatment groups: non-smokers, secondhand smokers, and smokers. Comprehensive assessment of all hormone levels: follicle-stimulating hormone (FSH), luteinizing hormone (LH), 17ß-oestradiol (E2), and progesterone (P), in the various phases of the menstrual cycle and with concomitant determinations of serum cotinine concentrations was performed. The menstrual cycle was observed with ultrasonography. RESULTS: Cigarette smoking may be an important factor in disrupting reproduction: 1. The increase in the oestradiol E2 level was accompanied by significantly lowered serum cotinine concentrations in tobacco smokers; 2. In smoking patients, the serum level of LH significantly increased on the first days of the menstrual cycle; 3. The higher levels of P (in the 14th and 21st days) were assumed to be the result of a longer menstrual cycle. CONCLUSIONS: Active and passive smoking may be an important contributor to reproductive health issues and deserves greater focus in health education programs directed towards women of reproductive age.

[Edwards syndrome--most frequent indications for genetic amniocentesis. Analysis of the last 5 years]. / Zespól Edwardsa--najczestsze wskazania do wykonania amniopunkcji genetycznych. Analiza na przestrzeni ostatnich 5 lat.

Edwards syndrome (trisomy 18) occurs in 1: 8000 live births and is closely related to the mother's age. Most of the embryos and fetuses with trisomy of 18 chromosome pair undergo natural abortion. Change in number and structure of chromosomes usually takes place spontaneously. However, the incidence of chromosome mutations increases with the presence of mutagenic factors. One of the chemical mutagenic factors is benzopyrene - present in cigarette smoke. Prenatal cytogenetic diagnostic is used for detecting diseases and clinical syndromes conditioned by chromosome aberrations. To this date the "golden standard" of this diagnostic is the assessment of the fetus karyotype by means of analysis of chromosome banding pattern from amniotic fluid-derived cells. The aim of the study was the analysis of indications for genetic amniocenteses carried out in the last 5 years and in case of which trisomy of chromosome 18 (Edwards syndrome) was diagnosed. The analysis covered 1593 results of fetus karyotypes obtained from Cytogenetic Laboratory of the Central Gynecological-Obstetric Clinical Hospital in Poznan over the last 5 years. The study procedure consisted in producing cell culture from amniotic fluid, appliance of appropriate color techniques and thorough microscopic analysis of chromosome banding pattern. As a result of the analysis it was discovered that in 1538 cases the karyotype was normal, and in 55 cases trisomy 18 was diagnosed, which constituted 3% of all cytogenetic tests. The highest number of trisomy 18 cases was noted in 2009 - 19 cases, which constitutes 5% of all tests. In 2010 and 2011 the results included respectively 2% and 3% of diagnosed trisomy 18 (Edwards syndrome). In the last 5 years normal results for karyotypes constituted 87%, in 10% cases other aberrations were diagnosed through cystogenetic tests, whereas 3% of the results have shown trisomy 18 (Edwards syndrome The most frequent indications for performing genetic amniocentesis, as a result of which trisomy 18 was diagnosed, were defects in ultrasound image, including fetal hydrops which constituted 27.3% of all indications. Malformation syndrome in fetus and hydramnion constituted only 9.1% of indications for cytogenetic tests where trisomy 18 was diagnosed. The highest incidence rate of trisomy 18 was diagnosed in fetuses of women aged between 30 and 34. These were followed by 29 fetuses with Edwards syndrome in mothers aged between 25 and 29.

[Frequency of prevalence of Turner syndrome in fetuses of patients referred to genetic amniocentesis in 2007-2011]. / Czestosc wystepowania zespolu Turnera u plodów pacjentek skierowanych na badanie amniopunkcji genetycznej w latach 2007-2011.

Turner syndrome is a genetic diseases caused by an aberration of sex chromosomes. It is conditioned by structural and/or quantitative aberration of one of the two X chromosomes, with frequent presence of mosaicism in cells. Since there are a few types of the syndrome, its diagnosis is often difficult and, as a consequence, a lot of people live without knowing of their disease. It is only during puberty that symptoms occur, or when full maturity begins it possible to diagnose the disease and start treatment. Genetic amniocentesis is a method thanks to which a material for cytogenetic test is obtained. The method involves puncturing amniotic sac and aspiration of fluid under the control of ultrasound for diagnostic purposes. Microscopic analysis of the chromosomes makes it possible to recognize aberration of one chromosome X which indicates Tuner syndrome phenotype. The objective of the study was the analysis of the frequency of prevalence of Turner syndrome in the patients' fetuses referred for genetic amniocentesis in 2007-2011. The most frequent cause of Turner syndrome in girls is missing one of two chromosomes X. the analysis shows that in 1815 tests Turner syndrome was confirmed in 46 cases which constitutes 2.5%. It is mostly young women, aged 25-29 that are at risk of having a child with this aberration. Indications which were later confirmed by the cases of fetuses with this syndrome included fetal hydrops, cystic hygroma and abnormalities in ultrasound image. In case of indications such as genetic defects in the family, incorrect result of triple test are not confirmed by Turner syndrome.

[Tobacco smoking influence on the level of sex hormones--animal model]. / Wplyw dymu tytoniowego na poziom hormonów plciowych--model zwierzecy.

Numerous studies warn that women who smoke can suffer from weakened functioning of their ovaries and disturbed synthesis and metabolism of hormones. This may cause many pregnancy complications or premature menopause and osteoporosis. Moreover, smoking disturbs the menstrual cycle, decreases the effectiveness and increases the undesirable effects of the hormone replacement therapy. Tobacco smoke disturbs gametogenesis, ovulation, Fallopian tube transport, fertilization and the implantation of a fertilized cell, which results in the reduction of fertility. The goal of the present thesis was a toxicological assessment of the influence of tobacco smoke on the level of luteinizing hormone, follicle stimulating hormone, progesterone, and estradiol in blood serum of female rats, taking into consideration the phases of their sexual cycle. The experiment utilized a cytological method of determining the phases of the sexual cycle, which enabled the researcher to divide the rats into two groups (exposed to tobacco smoke and unexposed). Each of the groups was further divided into four subgroups with six animals for each phase of the sexual cycle (Proestrus, Estrus, Metestrus, Diestrus). The rats from the first group were exposed to tobacco smoke with the concentration of 1500 mg of Carbon Monoxide (CO) per cubic meter of ambient air (per content of Carbon Monoxide) for 5 days for 6 hours a day. Every day before the exposition at the same time the phases of the sexual cycle of female rats were checked in all of the subgroups. On the last 5th day of the experiment, after the exposition to the smoke, smear tests were conducted. The unexposed group was the control group. The evaluation of the exposition of the animals to tobacco smoke was based on the determination of the level of cotinine in blood serum by ELISA method. The measurement of the concentration of hormones was conducted by means of a jurisdiction method of electrochemiluminescence. In the experiment, a statistical difference was observed between the concentration of cotinine in the blood serum of the animals that were in the Proesrtus phase (86.8 ng/ ml), compared to the group in the Metestrus phase (351.0 ng/ml) and Diestrus phase (304.6 ng/ml). In the experiment a very high level of progesterone concentration was marked in the blood serum of the female rats that were exposed to tobacco smoke and that were in the Proestrus phase (195.1 ng/ml). The level of progesterone among the animals exposed to cigarette smoke was statistically higher compared to the control group (99.1 ng/ml). In all probability, this was caused by the slower metabolism of nicotine or faster biotransformation of cotinine. The experiment confirmed the negative influence of cigarette smoke on the course of the sexual cycle. The sexual cycle of the female rats exposed to tobacco smoke changed its rhythm and kept its proper course only in 29% of the examined animals.

Interaction between tobacco smoke and alcohol in animal models.

This study aimed to evaluate the impact of nicotine and other xenobiotics contained in tobacco smoke on the pharmacokinetics of ethyl alcohol and on the levels of toxic ethanol metabolites such as acetic aldehyde.We also sought to evaluate the impact of a one-time administration of ethyl alcohol on the biotransformation of nicotine, the addictive alkaloid of tobacco smoke, to its main metabolite, cotinine. Rats were divided in three groups. The first group was exposed to tobacco smoke (6 h per day, for 5 days), the second group was treated with alcohol (2 g/kg), and the third group was exposed to tobacco smoke and treated with alcohol. Earlier exposure to tobacco smoke had an insignificant impact on the elimination of alcohol, but caused a significant increase in the volume of distribution, which could be caused by an increase in the first-pass effect. In contrast, inhaling tobacco smoke decreased acetic aldehyde concentrations in the first hour after alcohol administration. The major finding of this study was that a single dose of ethyl alcohol increases the rate of elimination of cotinine, the major metabolite of nicotine. This was demonstrated by a reduced biological half-life (t(0.5)) and mean resident time (MRT).