[ consequences of prenatal excess androgen exposure in anatomy of the reproductive system and physiology]

Introduction: The effects of environmental exposure during critical periods of gestational life on fetal growth and development have been confirmed by a large number of studies on human and animal models. Sex hormons are among the most influential environmental factor which affect on growth and development of different organs of fetus. Among them, androgens are the most important ones because they have various sources of production and secretion. Result previous studies that exposure to androgens during pregnancy may act as a teratogenic agent and cause defects, deministrated in offspring's endocrine and neural system developments. Considering the importance of this critical period for the development of some abnormal features in adulthood, basic research and clinical prevention efforts need to be run at this stage. This review article presents evidence on the effect of excessive androgens during fetal life on embryo development and evolution, which can lead to the development of certain phenotypes / diseases in adulthood

[ effects of prenatal excess androgens exposure on the gene expression]

Introduction: Prenatal exposure to excess androgens, as environmental factors affecting the fetal epigenome, and also a potent agent for developing special phenotypes in adulthood, has been the subject of many studies during recent decades. Results of various molecular studies conducted in this area indicate that exposure to androgens, during certain periods of growth and development of the fetus, affects cellular processes, tissues and organ development leading to phenotype and behavior alterations, one of which is causing susceptibility to polycystic ovary syndrome in adulthood. Testosterone, the most important androgen, has interfering effects in metabolic and endocrine pathways, usually a result of epigenetic changes. In recognition of diverted pathways leading to the development of disease conditions and considering possible interventions at the molecular level in these directions, control of prenatal environment and conditions can be taken to account as the first and most important step in prevention of related diseases. This article reviews the studies on the epigenetic and gene expression changes of various biological pathways as a result of this exposure, using the polycystic ovarian syndrome as an appropriate model to illustrate this exposure

[Association of polymorphisms G1193/C exon 8 and C2145/T exon 12 with anti-TPO titer in Iranian population]

Autoimmune thyroid diseases [AITD] are common and it is important to identify the genetic determinants. The aim of this study was to assess the relationship between two polymorphisms of Thyroid Peroxidase gene [TPO] and serum level of Anti-TPO titer in an Iranian population. We selected 184 individuals from Tehran Lipid and Glucose Study, categorized as the Anti-TPO- [n=72] and Anti-TPO+ [n=112] groups. Inclusion criteria for cases was Anti-TPO and Anti-Tg>100U/L with a history of hypothyroidism. Anti-TPO levels in subjects were measured by the ELISA kit. Genomic DNA was extracted using Saltingout/Proteinase K method. Polymorphism detection of Exon 8 and 12 was done using the PCR-RFLP method. The PCR products were incubated with restriction enzymes SacII and BsrI, respectively. The C allele frequency of C2145/T polymorphism Exon 12 [rs732608] was observed in 71.2% of patients and in 28.8% of normal individuals. This allele was significantly associated with increased levels of Anti-TPO [[T 140 +/- 330 pmol/L; vs. C 436 +/- 380 pmol/L; P<0.001], [OR: 9.2]]. The G1193/C was not associated with the level of serum Anti-TPO in this study. We demonstrated that the C allele polymorphism in C2145/T exon 12 is associated with high levels of serum Anti-TPO and that carriers of this allele are predisposed to disease 9.2 times more than those who do not have A allele