Polycystic ovary syndrome (PCOS) is one of the most common causes of infertility and metabolic problems among women of reproductive age. The mechanism of PCOS is associated with concurrent alterations at the hormonal level. The diagnosis assumes the occurrence of three interrelated symptoms of varying severity, namely ovulation disorders, androgen excess, or polycystic ovarian morphology (PCOM), which all require a proper therapeutic approach. The main symptom seems to be an increased androgen concentration, which in turn may contribute to different metabolic disorders. A number of papers have demonstrated the significant role of inositol therapy in PCOS. However, there is a lack of detailed discussion about the importance of myo-inositol (MI) and d-chiro-inositol (DCI) in reference to particular symptoms. Thus, the aim of this review is to present the effectiveness of MI and DCI treatment for PCOS symptoms. Moreover, the review is focused on analyzing the use of inositols, taking into account their physiological properties, together with the mechanism of individual PCOS symptom formation.

Polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT) and its metabo- lite, dichlorodiphenyldichloroethylene (DDE) can disturb the secretory function of the ovary and both contractions and secretory function of the uterus during the estrus cycle and pregnancy. Additionally, PCBs can pass through the placental barrier into allantoic and amniotic fluid. The presence of PCBs in these fluids is associated with higher frequency of spontaneous abortions and premature births in humans and animals. Therefore, the effect of PCBs, DDT and DDE on the connexins (Cx26, Cx32 and Cx43) and keratin 8 (KRT8) expression in bovine placentomes was investigated. The placentome slices from the second trimester of pregnancy were incubated with PCB153, 126, 77, DDT and DDE (each at doses of 1, 10 or 100 ng/ml) for 48 h. Then, the slices were stained using immunohistochemistry. The density of Cxs staining was measured with Axio- Vision Rel. 4.8 software in fetal-maternal connections and binuclear cells (BNC). None of the tested xenobiotics (XBs) affected the localization of Cxs and KRT8 in the fetal-maternal connec- tion area, but the XBs affected the density of Cxs in fetal-maternal connections and binuclear cells (BNCs). Depend on the doses, in fetal-maternal connections all used PCBs changed the protein expression of different Cxs, while in BNCs, all tested XBs except DDT increased the ex- pression of Cxs. None of investigated XBs affected on KRT8 expression. In summary, used XBs affect the expression of Cxs and change the quantitative relationships between them. Therefore, XBs can unfavorably influence function of the utero-placental barrier in cows.

Considering the properties of myo-inositol (MI) and D-chiro-inositol (DCI), which are well known in polycystic ovary syndrome therapy, and the limitations of adult granulosa cell tumor (AGCT) treatment, especially for androgen-secreting tumors, we studied the role of MI and DCI in the androgen-rich environment of AGCTs. For this purpose, we analyzed the mRNA expression of steroidogenic genes and the secretion of progesterone (P4) and 17β-estradiol (E2) in an unstimulated and/or dihydrotestosterone (DHT)-stimulated environment under MI and DCI influence. Thus, we used the HGrC1 and KGN cell lines as in vitro models of healthy and cancerous granulosa cells. We found that DHT, the most potent androgen, increased E2 secretion and steroidogenic acute regulatory protein (StAR) and cytochrome P450 side-chain cleavage gene (CYP11A1) mRNA expression without affecting 450 aromatase (CYP19A1) in AGCTs. However, after the MI and DCI treatment of KGN cells, both compounds strongly reduced StAR and CYP11A1 expression. Interestingly, in DHT-stimulated KGN cells, only DCI alone and its cotreatment with MI reduced both CYP11A1 mRNA and E2 secretion. These findings suggest that CYP11A1 is responsible for the antiestrogenic effect of DCI in the androgen-rich environment of AGCTs. Therefore, MI and DCI could be used as effective agents in the adjuvant treatment of AGCT, but further detailed studies are needed.