dinoprost and Polycystic-Ovary-Syndrome

Topics: Diagnosis, Differential; Dinoprost; Dysmenorrhea; Estrogens; Female; Hemorrhagic Disorders; Humans; Menorrhagia; Polycystic Ovary Syndrome; Prognosis; Uterine Diseases; Uterus; Vitamin B 6 Deficiency

We investigated the activities and relevance of a validated panel of antioxidant enzymes, cytokines, specific lipid peroxidation end products and six fatty acids by correlational analyses with peak E(2) levels and pregnancy outcome after ovarian stimulation for IVF or IUI.. Blood samples obtained from 15 patients undergoing ovarian stimulation with rFSH or hMG were divided into two groups. Group-1 was baseline blood collected on day-2-3 of women cycle. Group-2 is blood collected at the end of FSH/hMG injection. Serum was collected and stored in liquid nitrogen at -196 °C until analysis. Standard IVF and IUI procedures were followed. The serum levels of Paraoxonase (PON1), Superoxide Dismutases (SOD), Interleukin-6 (IL-6), Glutathione Peroxidase (GPx), 8-Isoprostane, and fatty acids Arachidic, Palmitic, Stearic, Oleic, Linoleic & Linolenic were measured.. With the exception of 8-Isoprostane, results showed a positive correlation between baseline and peak levels of E(2) and that of SOD, GPx, PON1, and IL-6. The PON1, IL-6 and SOD were significantly (p < 0.05) higher in pregnant than non-pregnant group. Fatty acid levels at baseline and peak E(2) were not different but pregnancy rates were found to be decreasing with higher palmitic, and stearic acid levels.. Ovarian stimulation causes a significant increase in serum PON1, SOD, GPx and IL-6 activity in women undergoing IVF or IUI. The high levels of IL-6, SOD, and PON1 and lower levels of palmitic, and stearic acids in the pregnancy positive group indicate that these oxidative stress and nutritional factors may be used as a predictive marker in controlled ovarian stimulation success.

Topics: Adult; Aryldialkylphosphatase; Biomarkers; Dinoprost; Endometriosis; Estradiol; Fatty Acids; Female; Fertilization in Vitro; Glutathione Peroxidase; Humans; Infertility, Female; Interleukin-6; Lipid Peroxidation; Ovulation Induction; Oxidative Stress; Polycystic Ovary Syndrome; Predictive Value of Tests; Pregnancy; Pregnancy Outcome; Pregnancy Rate; Prospective Studies; Sperm Injections, Intracytoplasmic; Superoxide Dismutase

Oxidative stress in the follicular fluid (FF) is thought to be responsible for the abnormal development of oocytes. In our study patients with polycystic ovarian syndrome (PCOS), endometriosis, and tubal infertility factor (TIF), and healthy women with a male factor of infertility, were prospectively enrolled. From each patient, a sample of individual FF was collected from a dominant follicle. Concentration levels of TAS, 8-IP, 8-OHdG, and AMH were determined. In women with PCOS, we found significantly lower values of oxidative stress markers in the FF. 8-IP and TAS levels were lower in the FF of women with endometriosis. In women with TIF, we also found significantly lower values of all tested markers in the FF, except for 8-OHdG and AMH. We wanted to see whether the biomarker measured in the FF in an individual diagnosis could predict a successfully obtained embryo from this particular follicle. The FF 8-OHdG result in PCOS patients stood out and proved to be a good predictive marker of matured and fertilized oocytes in these patients. Further research is needed to be able to apply the acquired knowledge in improving the outcome of IVF procedures.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Anti-Mullerian Hormone; Biomarkers; Dinoprost; Endometriosis; Female; Follicular Fluid; Humans; Infertility, Female; Live Birth; Oxidative Stress; Polycystic Ovary Syndrome; Pregnancy; Statistics, Nonparametric

To evaluate the plasma level of 8-isoprostanes in women with polycystic ovary syndrome. To also investigate whether there is a relationship between 8-isoprostanes and several cardiovascular risk factors.. A total of 125 women with polycystic ovary syndrome and 169 healthy women were enrolled in this case-control study. 8-Isoprostanes and different parameters were measured in all subjects. Patients were evaluated for the presence of polycystic ovary syndrome according to the Rotterdam Consensus Conference criteria.. 8-Isoprostanes levels were significantly higher in patients with polycystic ovary syndrome (138.4 ± 104.1 pg/mL) compared with control group (68.6 ± 34.3 pg/mL) (p < 0.001). The mean of triglycerides, lipid accumulation product, C-reactive protein, homocysteine, insulin, and homeostatic model assessment for insulin resistance were significantly higher in polycystic ovary syndrome patients with high 8-isoprostanes than those with normal 8-isoprostanes (p < 0.05). The Pearson correlation analyses showed that 8-isoprostanes levels in polycystic ovary syndrome group had a positive correlation with waist circumference, triglycerides, low-density lipoprotein cholesterol, apolipoprotein B, homocysteine, insulin, homeostatic model assessment for insulin resistance.. Patients with polycystic ovary syndrome have higher 8-isoprostanes levels and it is associated with several cardiovascular risk factors.

Topics: Adult; Biomarkers; Cardiovascular Diseases; Case-Control Studies; Dinoprost; Female; Humans; Isoprostanes; Obesity; Polycystic Ovary Syndrome; Risk Factors; Young Adult

To investigate the role of oxidative stress in pathogenesis of polycystic ovary syndrome (PCOS), especially in the obese PCOS.. 43 PCOS patients with BMI > or = 23 kg/m2 were grouped into PCOS1. 42 PCOS patients with BMI < 23 kg/m2 were grouped into PCOS2. Meanwhile, 85 infertility patients with normal endocrine function and body weight were grouped into control group. All patients were subjected to the measurement of serum levels of superoxide dismutase (SOD), 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) and visfatin. The difference among PCOS1, PCOS2 and control group were compared and the relationships between the indexes were analyzed with simple liner regression analysis.. The serum level of SOD in PCOS1 and PCOS2 were lower than that in the control group (P < 0.05), and the serum level of SOD in PCOS1 was lower than that in PCOS2 (P < 0.05). The serum levels of 8-iso-PGF2alpha and visfatin in PCOS1 were higher than those in PCOS2 and control group (P < 0.05). The serum levels of 8-iso-PGF2alpha and visfatin between PCOS2 and control group were not statistical different. In PCOS1 and PCOS2 groups, SOD activity decreased with increasing levels of 8-iso-PGF2alpha, the regression coefficient was -0.407. For serum vifation, there were positive correlations with both BMI and 8-iso-PGF2alpha, but negative correlation with SOD; the coefficients were 0. 402 (P = 0.008), 0.612 (P = 0.000), and -0.153 (P = 0.000), respectively. The indexes mentioned above did not have the liner relationship in the control group.. There was oxidative stress in PCOS patients, which was not obvious in the normal weight PCOS patients but quite severe in the obese PCOS patients.

Topics: Adolescent; Adult; Dinoprost; Female; Humans; Nicotinamide Phosphoribosyltransferase; Obesity; Oxidative Stress; Polycystic Ovary Syndrome; Regression Analysis; Superoxide Dismutase; Young Adult

The present study investigated the role of the N, N'-dimethylbiguanide metformin (50 mg/kg body weight in 0.05 ml water, given orally with a canulla) in preventing the adverse effects generated by hyperandrogenism on uterine function. Daily injection of dehydroepiandrosterone (DHEA: 6 mg/100 g body weight in 0.1 ml oil) for 20 consecutive days induces polycystic ovaries in BALB/c mice. In this model we found that DHEA produced alterations on uterine histology closely related to the development of pre-cancerous structures concomitantly with increased incidence of uterine apoptosis. The injection of DHEA induced a pro-inflammatory status since uterine prostaglandin (PG) F2 alpha levels and cyclooxygenase 2 were increased although PGE levels were decreased. Furthermore, DHEA promoted a pro-oxidant status since it increased nitric oxide synthase (NOS) activity and decreased superoxide dismutase and catalase activities and the antioxidant metabolite glutathione levels. DHEA also regulated the percentages of CD4+ and CD8+ T lymphocyte that infiltrate uterine tissue. When metformin was administered together with DHEA uterine histology and apoptosis did not differ when compared with controls. Therefore, metformin prevented the pro-inflammatory and pro-oxidative status generated by DHEA and restores the ratios of CD4+ and CD8+ T cells to those observed in controls. We conclude that metformin is able to restore either directly or indirectly uterine function by preventing some inflammatory and oxidative alterations produced by hyperandrogenism.

Topics: Animals; Blotting, Western; Catalase; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cyclooxygenase 2; Dehydroepiandrosterone; Dinoprost; Enzyme Activation; Female; Flow Cytometry; In Vitro Techniques; Metformin; Mice; Mice, Inbred BALB C; Nitric Oxide Synthase; Oxidative Stress; Polycystic Ovary Syndrome; Radioimmunoassay; Superoxide Dismutase; Uterus

The aim of the present work was to study some of the adverse effects produced by hyperandrogenism on the uterine function. Daily injection of dehydroepiandrosterone (DHEA: 6 mg/ 100 g body weight, sc) for 20 consecutive days induced polycystic ovaries in BALB/c mice. In this model, we found that DHEA produced alterations on uterine histology closely related to the development of tumour structures. In addition, hyperandrogenism induced a pro-inflammatory and a pro-oxidant condition represented by increased levels of prostaglandin F2 alpha production and uterine nitric oxide synthase (NOS) activity and by a decrease in both superoxide dismutase (SOD) and catalase (CAT) activities together with a decrease in the levels of the antioxidant metabolite glutathione (GSH). DHEA also induced an increase in CD4+ together with a decrease in the CD8+ T lymphocytes that infiltrate the uterine tissue. We conclude that this intricate network of regulators could be responsible for the low rate of implantation observed in women with polycystic ovary syndrome.

Topics: Adjuvants, Immunologic; Animals; Catalase; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cyclooxygenase 1; Cyclooxygenase 2; Dehydroepiandrosterone; Dinoprost; Female; Glutathione; Hyperandrogenism; Membrane Proteins; Mice; Mice, Inbred BALB C; Nitric Oxide Synthase; Ovary; Oxidative Stress; Polycystic Ovary Syndrome; Prostaglandins E; Superoxide Dismutase; Uterus

This study examines the effect of a 6 month dietary supplement of either gamma-linolenic acid (GLA) or eicosapentaenoic acid (EPA) on the synthesis of prostaglandins E2 and F2 alpha by the endometrium of women with regular menstrual cycles. Samples of endometrium, obtained pre- and post-treatment, were incubated in vitro for 2 h and the prostaglandins E2 and F2 alpha released into the medium measured by radioimmunoassay. The ability of the tissue to take up 14C-arachidonic acid before and after treatment was also examined. Both GLA and EPA caused a marked decrease in the synthesis of prostaglandins E2 and F2 alpha (P < 0.001) but under the experimental conditions used, there was no consistent effect on arachidonic acid uptake. Body mass index, serum testosterone, fasting insulin and serum sex hormone-binding globulin (SHBG) concentrations did not change during the 6 month treatment period. An effect of GLA and EPA on arachidonic acid uptake into endometrial tissue explants was demonstrated in vitro. In the presence of both GLA and EPA, uptake into phospholipids (particularly phosphatidylcholine) decreased while uptake into triglycerides increased. Free 14C-arachidonic acid levels (that which could not be removed from the tissue by washing) also increased. Suppression of endometrial prostaglandin E2 and F2 alpha synthesis following GLA or EPA supplementation can be explained as direct competition between these fatty acids and arachidonic acid (the precursor of 2-series prostaglandins) for incorporation into membrane phospholipids. The amount of arachidonic acid available for 2-series prostaglandin synthesis will therefore be reduced. However, other mechanisms may exist which need to be investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Arachidonic Acid; Biological Transport; Dietary Fats; Dinoprost; Dinoprostone; Eicosapentaenoic Acid; Endometrium; Female; gamma-Linolenic Acid; Humans; Insulin; Membrane Lipids; Organ Culture Techniques; Phospholipids; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin; Testosterone; Triglycerides