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PubMed1997

Neurodevelopment in offspring of hairdressers.

The hypothesis that intrauterine exposure to hairdressers' chemicals adversely affects neurodevelopment of the offspring was investigated. Neurodevelopmental characteristics were analysed using a historical cohort study of reproductive disorders among hairdressers in The Netherlands. Because exposure in hair salons to agents toxic to reproductive processes might have changed over time, two specific study periods were examined: from 1986 to 1988 and from 1991 to 1993. Nine thousand hairdressers and 9000 clothing sales clerks (referent group) who were in the reproductive age in the defined study periods were selected by the trade association for service jobs. Frequency matching assured comparability with regard to age. All women were invited by mail to complete a short self-administered questionnaire on their reproductive history, including questions on the ages of their child at the times of the first words, first sentences, and first steps, and the occurrence of seizures during fever. The results showed that in 1986 to 1988 more children of hairdressers started speaking their first words after 15 months and their first sentences after 24 months. For 1991 to 1993 no increased risks of these outcomes were found. Seizures during fever had occurred more often among children of hairdressers in 1986 to 1988, and in 1991 to 1993, especially when women had been working until maternity leave. Although the quality of the data in this explorative study requires careful interpretation, the consistent results seem to indicate adverse effects on neurodevelopment among offspring of hairdressers in the earlier years (1986 to 1988). In the later years the effect seemed to be disappearing. However, these findings should be confirmed in more detailed studies.

Child, Preschool↗
PubMed2003

Proliferation and functional maturation of Sertoli cells, and their relevance to disorders of testis function in adulthood.

Disorders of testicular function may have their origins in fetal or early life as a result of abnormal development or proliferation of Sertoli cells. Failure of Sertoli cells to mature, with consequent inability to express functions capable of supporting spermatogenesis, is a prime example. In a similar way, failure of Sertoli cells to proliferate normally at the appropriate period in life will result in reduced production of spermatozoa in adulthood. This review focuses on the control of proliferation of Sertoli cells and functional maturation, and is motivated by concerns about 'testicular dysgenesis syndrome' in humans, a collection of common disorders (testicular germ-cell cancer, cryptorchidism, hypospadias and low sperm counts) which are hypothesized to have a common origin in fetal life and to reflect abnormal function of Sertoli (and Leydig) cells. The timing of proliferation of Sertoli cells in different species is reviewed, and the factors that govern the conversion of an immature, proliferating Sertoli cell to a mature, non-proliferating cell are discussed. Protein markers of maturity and immaturity of Sertoli cells in various species are reviewed and their usefulness in studies of human testicular pathology are discussed. These markers include anti-Mullerian hormone, aromatase, cytokeratin-18, GATA-1, laminin alpha5, M2A antigen, p27(kip1), sulphated glycoprotein 2, androgen receptor and Wilms' tumour gene. A scheme is presented for characterization of Sertoli-cell only tubules in the adult testis according to whether or not there is inherent failure of maturation of Sertoli cells or in which the Sertoli cells have matured but there is absence, or acquired loss, of germ cells. Functional 'de-differentiation' of Sertoli cells is considered. It is concluded that there is considerable evidence to indicate that disorders of maturation of Sertoli cells may be a common underlying cause of human male reproductive disorders that manifest at various life stages. This recognition emphasizes the important role that animal models must play to enable identification of the mechanisms via which failure of proliferation and maturation of Sertoli cells can arise, as this failure probably occurs in fetal life.

Adult↗
PubMed1989

Pharmacologic therapy of male infertility: specific treatment.

Pharmacotherapy of male reproductive disorders is applicable to the majority of men seeking treatment for infertility. Since a favorable prognosis is associated with specific medical measures directed toward enhancing sperm quality, a comprehensive clinical and laboratory assessment of the infertile male is essential. This treatment may consist of replacement therapy for pituitary or hypothalamic dysfunction (i.e., exogeneous gonadotropins or GnRH), suppression of prolactin excess, antimicrobial therapy, sympathomimetic agents for ejaculatory disorders, or immunosuppressive treatment of sperm autoimmunity. Finally, the possibility of multiple causes of male reproductive dysfunction and their specific forms of treatment should be considered.

Humans↗
PubMed2001

Sex-change chemicals and their influence on the brain.

The potential for man-made chemicals to mimic or antagonise natural hormones is a controversial issue, but one for which increasing amounts of evidence are being gathered worldwide. The controversy surrounds not so much the matter of whether these chemicals can mimic hormones in vitro--this phenomenon has been widely accepted in the scientific world - but more whether, as a result, they can disrupt reproduction in a wildlife situation. It has, nevertheless, been acknowledged that many wildlife populations are exhibiting reproductive and/or developmental abnormalities such as intersex gonads in wild roach populations in the U.K. and various reproductive disorders in alligators in Lake Apopka, Florida. However, the causative agents for many of these effects are difficult to specify, due to the extensive mixtures of chemicals--each of which may act via different pathways--to which wild populations are exposed, together with the wide variability observed even in natural (uncontaminated) habitats. As a result, any information detailing fundamental mechanism of action of the so-called endocrine disrupting chemicals (EDCs) is of use in determining whether or not these chemicals, as they are present in the environment, may in fact be capable of causing some of the effects observed in wildlife over recent years.

Animals↗
PubMed2006

Insulin resistance, the metabolic syndrome, diabetes, and cardiovascular disease risk in women with PCOS.

Polycystic ovary syndrome is the most common endocrinopathy of reproductive aged women affecting 6-10% of the population. Traditionally considered a reproductive disorder manifesting as chronic anovulation, infertility, and hyperandrogenism, management has primarily focused on short-term reproductive outcomes. Recently, however, significant metabolic aspects in conjunction with longer-term health sequealae of PCOS have been recognized. The metabolic features are primarily related to underlying insulin resistance (IR), which is now understood to play an important role in both the pathogenesis and long-term sequelae of PCOS.

Cardiovascular Diseases↗
PubMed1993

Exposure to ethylene glycol ethers and spermatogenic disorders in man: a case-control study.

A case-control study was conducted among first time patients at a clinic for reproductive disorders. The study group consisted of 1019 cases, defined as patients diagnosed infertile or subfertile on the basis of a spermiogram and 475 controls who were diagnosed as normally fertile by the same procedure. Possible exposure to ethylene glycol ethers was assessed by the presence of the urinary metabolites methoxyacetic acid (MAA) and ethoxyacetic acid (EAA) respectively for 2-methoxyethanol and 2-ethoxyethanol or their acetates. In total, EAA was detected in 39 cases and six controls, with a highly significant odds ratio of 3.11 (p = 0.004). On the other hand, MAA was only found in one case and two controls. The presence of EAA in urine proved to be strongly associated with exposure to preparations containing solvents, especially paint products, and with some groups of occupations, the most important of which were also directly or possibly connected with paint products. The absence of a significant correlation between the concentration of urinary EAA and the various measures of sperm quality could be explained by the expected latent period between exposure and observed effects. Other temporal aspects of the relation between exposure as judged from the presence of urinary EAA and diagnosis are also discussed.

Acetates↗
PubMed2005

Endogenous estrogens inhibit mouse fetal Leydig cell development via estrogen receptor alpha.

It is now accepted that estrogens play a role in male fertility and that exposure to exogenous estrogens during fetal/neonatal life can lead to reproductive disorders in the male. However, the estrogen receptor (ER)-mediated processes involved in the regulation of male reproduction during fetal and neonatal development are still largely unclear. We previously reported that ER beta deficiency affects gametogenesis in mice but changes neither the number nor the differentiated functions of fetal Leydig cells. We show here that ER alpha-deficient mice (ER alpha-/-) display higher levels of testicular testosterone secretion than wild-type mice from fetal d 13.5 onwards. This results from higher levels of steroidogenic activity per fetal Leydig cell, as indicated by the hypertrophy of these cells and the higher levels of mRNA for StAR, P450c17 and P450scc in the testis, for a similar number of Leydig cells. Because LH is not produced on fetal d 13.5 and because no change in plasma LH concentration was observed in 2-d-old ER alpha-deficient mice, LH is probably not involved in the effects of estrogens on testicular steroidogenesis in fetal and early neonatal Leydig cells. Furthermore, inactivation of ER beta did not change the effect of ER alpha inactivation on steroidogenesis. Lastly, in an organ culture system, 1 mum diethylstilbestrol decreased the testosterone secretion of wild-type fetal and neonatal testes but not of ER alpha-/- testes. Thus, this study shows that endogenous estrogens physiologically inhibit steroidogenesis via ER alpha by acting directly on the testis early in fetal and neonatal development.

Animals↗
PubMed1999

[Reproductive performance and milk production of Israeli-Holstein cows with different supplementation during the dry period].

In three field trials comprising 602 Israeli-Holstein dairy cows, the effect of the dry period ration on reproductive performance, culling rate and milk production was investigated. The cows were fed in groups. The basic dry period rations consisted for two herds of medium quality cereal hay and for one herd of corn straw, which were fed ad libitum. In each herd dry cows were assigned to an experimental and control group. Cows of the experimental group were supplemented with 1.5 to 3 kg of lactating cows mixed ration (LMR), whereas in the control group the amount of supplement was increased by the factor two or 3.3. In the experimental group the amount of the supplement was calculated to achieve levels of net energy and of crude protein close to NRC requirements; in the control group the level of net energy and protein was 12 to 18% higher as compared to the experimental group. The amount of LMR supplement in the experimental group of herds A, B, C were 1.5 kg, 1.9 kg, and 3 kg, respectively. In the control groups these amounts were 5 kg, 3.8 kg, and 6 kg, respectively. The groups fed moderate amounts of LMR supplement had a higher conception rate at first insemination, a higher percentage of cows conceiving and fewer cows culled in the consecutive lactation than cows fed increased amounts of LMR supplement. The lactational incidence of reproductive disorders and the milk production were not affected by the differences in feeding during the dry period. Reproductive performance and culling rate appeared to be more favorable for cows fed moderate amounts of supplement during the entire dry period or during the last 3 to 4 weeks of the dry period.

Animal Feed↗
PubMed1994

Reproductive manifestations of thyroid disease.

Thyroid function and reproductive function have many interactions, the scope and mechanism of which are not fully understood. These functions are of greatest clinical importance for veterinarians working with breeders of purebred dogs. Thyroid dysfunction does not always result in clinical signs of reproductive disorders or in subfertility. It seems that animals with overt thyroid dysfunction are those most likely to manifest reproduction problems.

Animals↗
PubMedDate not supplied

Evaluation of testicular toxicity in safety evaluation studies: the appropriate use of spermatogenic staging.

Toxicology of the male reproductive system has received increased interest in recent years partly fuelled by the growing reports of falling sperm counts and rising reproductive disorders in the human population. Recently revised regulatory guidelines for the safety assessment of pharmaceuticals and chemicals on reproduction and fertility have emphasized the importance of detailed histopathological examination of the testes as a sensitive method for detecting disturbances in spermatogenesis. Unfortunately this has been accompanied by a general confusion regarding a practical approach to undertaking such a detailed examination, particularly in respect to the use of spermatogenic or tubular staging to identify subtle disturbances in spermatogenesis. The ability to identify tubular stages of the spermatogenic cycle in sections of testis plus a good understanding of the spermatogenic process and its dynamics are essential in order to carry out a sensitive of testicular histopathology and to interpret the changes seen. A rational approach is required initially to detect and subsequently to characterize toxic effects to the male reproductive system. It is important that a distinction is made between these two objectives since different study designs are required and different methodology may be employed to produce the type of information or data required.

Animals↗
PubMed1991

[Detection of residues of foreign substances in the tissues of cows and bulls and in bull sperm].

The presence of residues of some chemical foreign substances in the tissues of cow and bull genitals and in sire sperm was investigated due to frequently occurring reproductive disorders in some large cow herds, mainly with the large-scale rearing system. Negative effects of these substances on the reproductive process of cows and bulls were supposed to be exerted. In keeping with the opinions and data mentioned by some authors in the literature there is a fact that the sperm and tissues of genitals belong to those biological materials which are the first to respond to the toxic effects of different chemicals by disorders of their physiological functions. These disorders, mainly in sperm cells, can be evaluated objectively from the recorded changes in physical and biological characteristics. The chemicals under investigation were residues of hexachlorobenzene (HCB), alpha, beta, gamma hexachlorocyclohexane isomers, sigma DDT and its metabolites and of polychlorinated biphenyls (PCB). The concentrations of the residues of these substances in the examined biological materials were very low, in some cases they were not detected at all. It is therefore supposed that these residues could not exert and significant effects on the physiological functions of examined cows and bulls with respect to their reproductive organs. These examinations should become more extensive and thorough, mainly in the herds and regions exposed to potential contamination; the residues of foreign substances should be investigated in view of ecological conditions. These postulates are very urgent, as illustrated by the literature data: in some cases negative effects of certain foreign substances (PCB) were found out and demonstrated on the reproductive functions of people and farm animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Insulin-lowering agents in the management of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a medical condition that has brought multiple specialists together. Gynecologists, endocrinologists, cardiologists, pediatricians, and dermatologists are all concerned with PCOS patients and share research data and design clinical trials to learn more about the syndrome. Insulin resistance is a common feature of PCOS and is more marked in obese women, suggesting that PCOS and obesity have a synergistic effect on the magnitude of the insulin disorder. Hyperinsulinemia associated with insulin resistance has been causally linked to all features of the syndrome, such as hyperandrogenism, reproductive disorders, acne, hirsutism, and metabolic disturbances. Women with PCOS should be evaluated for cardiovascular risk factors, such as lipid profile and blood pressure. Modification of diet and lifestyle should be suggested to those who are obese. Several insulin-lowering agents have been tested in the management of PCOS. In particular, metformin is the only drug currently in widespread clinical use for treatment of PCOS. In a high percentage of patients, treatment with metformin is followed by regularization of menstrual cycle, reduction in hyperandrogenism and in cardiovascular risk factors, and improvement in response to therapies for induction of ovulation.

Female↗
PubMedDate not supplied

[Detection of viral-bacterial factors responsible for infertility in couples].

A high prevalence of genital infections was revealed in patients suffering for a long time from sterility. The inflammatory process was found to predominate in tubal sterility. In other forms of sterility with asymptomatic urogenital infections the couples are frequently unaware of the disease and are not properly examined. Genital inflammations not diagnosed for many years augment the endocrine disorders and stimulate the development of autoimmune states. Today, a mixed viral/bacterial urogenital infection is the principal cause of reproductive disorders.

Female↗
PubMedDate not supplied

Mood disorders and the reproductive cycle.

Women have a significantly higher risk for developing mood disorders than men. Although reasons for this gender difference are not fully understood, it is clear that changing levels of reproductive hormones throughout women's life cycles can have direct or indirect effects on mood. Fluctuations in reproductive hormones may interactively affect neuroendocrine, neurotransmitter, and circadian systems. Reproductive hormones also may affect response to some antidepressant drugs and alter the course of rapid-cycling mood disorders. Nonpharmacologic interventions, such as light therapy and sleep deprivation, may be beneficial for mood disorders linked to the reproductive cycle. These interventions may have fewer side effects and a greater potential for patient compliance than some antidepressant drugs.

Female↗
PubMed2001

Hormones and testis development and the possible adverse effects of environmental chemicals.

Development of a fetus into a phenotypic male depends, first, on testis formation and second, on hormone production by the fetal testis. Disorders of testicular hormone production or action can lead in severe cases to phenotypic abnormalities or can predispose towards impaired reproductive health. Evidence for deteriorating human male reproductive health, especially an increase in testicular cancer, points to disturbed (hormonal) development of the fetal testis. By comparison of testicular dysgenesis in humans and exposure to certain phthalates in fetal rats, the similarities in outcomes and testicular cell-cell disruption are highlighted as are the pathways via which oestrogenic and (especially) anti-androgenic environmental chemicals might act to induce such changes. The susceptibility of sperm production in adulthood to 'hormonal' disruption in fetal and neonatal life is also discussed. Though it is concluded that no direct evidence links human exposure to environmental chemicals and male reproductive disorders that stem from disturbed testis development, this is based mainly on lack of information. Using the example of phthalates, for which new data have emerged, it is argued that until the appropriate in vivo studies are undertaken, the safety of hormonally active environmental chemicals, especially in mixtures, will continue to give cause for concern as far as testicular development is concerned.

Animals↗
PubMed1999

Increased prevalence of luteinizing hormone beta-subunit variant in patients with premature ovarian failure.

OBJECTIVE: To evaluate the significance of an LH variant with a mutant beta-subunit (Trp8 to Arg8 and Ile15 to Thr15) in gynecologic disease, including infertility. DESIGN: Clinical study. SETTING: Department of Obstetrics and Gynecology, Shimane Medical University Hospital, Izumo, Japan. PATIENT(S): Two hundred forty-five Japanese women with endocrine disorders and/or gynecologic disease and 153 healthy, nonpregnant, fertile Japanese women. INTERVENTION(S): A blood sample was collected. MAIN OUTCOME MEASURE(S): The ratio of LH values from the SPAC-S and Immulyze assays (LH ratio: SPAC-S LH/Immulyze LH) was used to determine variant (< or =0.5) or wild-type (>0.5) LH status according to a demonstrated relation between the ratio and the sequence of the LH beta-subunit gene. RESULT(S): The LH ratio was lower (0.80+/-0.31) in the 245 patients than in the controls (1.00+/-0.38), and the variant was more frequent in the patients (18.4%) than in the controls (8.5%). We found no difference in the frequency of the variant between infertile and fertile patients. The prevalence of infertility did not differ between patients with variant LH and patients with normal LH. Ovulatory disorders, hyperprolactinemia, premature ovarian failure, menstrual disorders, and luteal insufficiency were significantly more frequent in patients with the variant. CONCLUSION(S): Variant LH may contribute to female reproductive disorders, including infertility and premature ovarian failure.

Adolescent↗
PubMed2002

The effect of metformin on hirsutism in polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is a common reproductive disorder characterised by insulin resistance and often associated with hirsutism. Insulin sensitising agents, such as metformin, improve both the biochemical and reproductive parameters; however, no study has been designed to specifically assess the effect of metformin on hair growth. DESIGN AND PATIENTS: Sixteen women with PCOS and hirsutism were enrolled into a 14 month (two 6 month phases with a 2 month washout) double-blind placebo-controlled cross over study. MEASUREMENTS: Hirsutism was assessed using the Ferriman and Gallwey (F-G) score, patient self-assessment and growth velocity. Weight, height and waist-hip ratio were recorded. Gonadotrophins, androgens, plasma glucose and lipids were also measured. RESULTS: Ten women completed the full 14 month study. There was a significant improvement in hirsutism at the end of the metformin phase compared with placebo: F-G score 15.8+/-1.4 vs 17.5+/-1.2 (P=0.025) and patient self-assessment 2.4+/-0.1 vs 3.3+/-0.3 (P=0.014). Growth velocity, in millimetres per day at the end of each phase also improved (0.67+/-0.17 vs 0.77+/-0.11; P=0.03). There was a non-significant improvement in both sex hormone binding globulin (SHBG) and free androgen index (FAI), although there was a significant difference between baseline and metformin treatment for SHBG (P=0.023) and FAI (P=0.036). Metformin treatment also reduced weight significantly (91.5+/-7.6 vs 94.0+/-9.8 kg; P=0.009) and led to a significant improvement in cycle frequency (0.53+/-0.12 vs 0.35+/-0.08 cycles per month; P=0.008). CONCLUSION: We have demonstrated that metformin treatment in a group of women with PCOS results in a clinically and statistically significant improvement in hair growth compared with placebo.

Body Constitution↗
PubMed1994

Mechanisms of reproductive deficiency in male rats treated neonatally with a gonadotrophin-releasing hormone antagonist.

It is well known that males injected neonatally with oestradiol or antiserum or antagonists (ANT) against gonadotrophin-releasing hormone (GnRH) show multiple reproductive disorders. In the present work, in males treated neonatally with GnRH-ANT, we have analysed: (1) whether the impairment of reproductive function can be blocked by simultaneous treatment with gonadotrophins, (2) the possible differences in the effects of GnRH-ANT injected before or after the proliferation of Sertoli cells which takes place between days 1 and 15 of age, and (3) the mechanism(s) for the increased FSH secretion observed in adulthood. Experimental designs included: administration of GnRH-ANT between days 1 and 16 or 15 and 30 of age, simultaneous administration of gonadotrophins and GnRH-ANT to neonatal males, and measurement of FSH secretion after orchidectomy or specific destruction of Leydig cells with ethylene dimethane sulphonate (EDS) in adult males treated neonatally with GnRH-ANT. The principal new data presented in our studies are the following: (1) delayed puberty was observed not only in males injected neonatally with GnRH-ANT, but also in those injected with gonadotrophins or with GnRH-ANT and gonadotrophins, (2) the decreased fertility and increased FSH secretion observed in adult males treated neonatally with GnRH-ANT were normalized by simultaneous administration of GnRH-ANT and gonadotrophins, and (3) the increased FSH secretion in adult males treated neonatally with GnRH-ANT remained after EDS or orchidectomy, suggesting that mechanisms other than decreased inhibin secretion were involved in the increased secretion of FSH.

Animals↗