Altered mitochondrial homeostasis on bisphenol-A exposure and its association in developing polycystic ovary syndrome: A comprehensive review.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrinopathy that is known to be one of the most common reproductive pathologies observed in premenopausal women around the globe and is particularly complex as it affects various endocrine and reproductive metabolic pathways. Endocrine-disrupting chemicals (EDCs) are considered to be environmental toxicants as they have hazardous health effects on the functioning of the human endocrine system. Among various classes of EDCs, bisphenol A (BPA) has been under meticulous investigation due to its ability to alter the endocrine processes. As there is emerging evidence suggesting that BPA-induced mitochondrial homeostasis dysfunction in various pathophysiological conditions, this review aims to provide a detailed review of how various pathways associated with ovarian mitochondrial homeostasis are impaired on BPA exposure and its mirroring effects on the PCOS phenotype. BPA exposure might cause significant damage to the mitochondrial morphology and functions through the generation of reactive oxygen species (ROS) and simultaneously downregulates the total antioxidant capacity, thereby leading to oxidative stress. BPA disrupts the mitochondrial dynamics in human cells by altering the expressions of mitochondrial fission and fusion genes, increases the senescence marker proteins, along with significant alterations in the mTOR/AMPK pathway, upregulates the expression of autophagy mediating factors, and downregulates the autophagic suppressor. Furthermore, an increase in apoptosis of the ovarian granulosa cells indicates impaired folliculogenesis. As all these key features are associated with the pathogenesis of PCOS, this review can provide a better insight into the possible associations between BPA-induced dysregulation of mitochondrial homeostasis and PCOS.

Distinct metabolic signatures in blood plasma of bisphenol A-exposed women with polycystic ovarian syndrome.

Polycystic ovarian syndrome (PCOS) is a complicated endocrinopathy with an unclear etiology that afflicts fertility status in women. Although the underlying causes and pathophysiology of PCOS are not completely understood, it is suspected to be driven by environmental factors as well as genetic and epigenetic factors. Bisphenol A (BPA) is a weak estrogenic endocrine disruptor known to cause adverse reproductive outcomes in women. A growing relevance supports the notion that BPA may contribute to PCOS pathogenesis. Due to the indeterminate molecular mechanisms of BPA in PCOS endocrinopathy, we sought liquid chromatography with tandem mass spectrometry (LC-MS/MS), a metabolomics strategy that could generate a metabolic signature based on urinary BPA levels of PCOS and healthy individuals. Towards this, we examined urinary BPA levels in PCOS and healthy women by ELISA and performed univariate and chemometric analysis to distinguish metabolic patterns among high and low BPA in PCOS and healthy females, followed by pathway and biomarker analysis employing MetaboAnalyst 5.0. Our findings indicated aberrant levels of certain steroids, sphingolipids, and others, implying considerable disturbances in steroid hormone biosynthesis, linoleic, linolenic, sphingolipid metabolism, and various other pathways across target groups in comparison to healthy women with low BPA levels. Collectively, our findings provide insight into metabolic signatures of BPA-exposed PCOS women, which can potentially improve management strategies and precision medicine.

Bisphenol A exposure modulates reproductive and endocrine system, mitochondrial function and cellular senescence in female adult rats: A hallmarks of polycystic ovarian syndrome phenotype.

Bisphenol A (BPA) mimics estrogen and consequently suspected to be detrimental to female reproductive system. Biomonitoring confirms the BPA burden in body leading to a complex condition called polycystic ovarian syndrome (PCOS) which is frequently attributed to female infertility. Due to unclear precise molecular pathomechanisms of BPA in PCOS, we intend to examine the molecular mechanisms of the reproductive, endocrine, mitochondrial features, and cellular senescence in BPA-treated rats. We analyzed vaginal smears and ovarian follicles using microscope, assessed sex hormones by ELISA, analyzed BPA target gene expression by semi-quantitative RT-PCR, assessed senescence induction by ß-galactosidase staining and immunofluorescence in BPA-treated rats. Our data showed hormonal imbalance, impaired folliculogenesis, abnormal expression patterns of target genes, CDKN2A overexpression and enhanced ROS levels in BPA-treated rats. This study provides insights on the effects of BPA exposure on ovulatory, hormonal, mitochondrial dysfunction, and senescence that benefit in better understanding of PCOS induced by BPA.

Effectiveness of antepartum breathing exercises on the outcome of labour: A randomized controlled trial.

Background Childbirth is a life-transforming intense event to a woman and her family. Even though a variety of non-pharmacological techniques are readily available to alleviate the distress of women in labour, the majority of women are unaware of its benefits. The objective of the study was to explore the impact of a simple non-pharmacological technique i.e., antepartum breathing exercises on maternal outcomes of labour among primigravid women. Methods A single centre prospective, single-blinded, randomized controlled trial was conducted at the antenatal outpatient clinic of a secondary healthcare institution. Eligible primigravid women were randomized into intervention and standard care groups. Both groups received standard obstetrical care. In addition, the intervention group were taught antepartum breathing exercises and were advised to practise daily and also during the active stage of labour. The primary outcome of the trial was the maternal outcome of labour measured in terms of onset of labour, nature of delivery, duration of labour, and need for augmentation of labour. Data was collected using World Health Organization (WHO) partograph, structured observational record on the outcome of labour. Results A total of 98 (70%) primigravid women who practised antepartum breathing exercises had spontaneous onset of labour. The odds of spontaneous onset of labour after randomization in the intervention group was 2.192 times more when compared to standard care at a (95% confidence interval 1.31-3.36, p<.001). Also, the requirement for augmentation of labour was minimal and there was a reduction in the rate of caesarean deliveries ( p <.05) based on the χ2 test. The overall mean duration of labour was less compared to standard care group F(1)= 133.800, p <.001. Conclusion Antepartum breathing exercises during labour can facilitate spontaneous vaginal birth, shorten the duration of labour, and reduce the need for operative interference.

Community-Based Prevalence of Genital Human Papilloma Virus (HPV) Infection: a Systematic Review and Meta-Analysis

Introduction: Cervical cancer probably represents the best-studied human cancer caused by a viral infection and the causal association of this preventable cancer with human papilloma virus (HPV) is well established. Worldwide there is a scarcity of data regarding HPV prevalence with vast differences existing among populations. Objective: The aim of this meta-analysis was to determine the community-based HPV prevalence estimates among asymptomatic women from urban and rural set ups and in participants of cancer screening clinics. Study design: Systematic review and meta-analysis. Methods: PubMed-Medline, CINAHL, Scopus, and Google scholar were systematically searched for studies providing prevalence data for HPV infection among asymptomatic women between 1986 and 2016. Results: The final analysis included 32 studies comprising a population of 224,320 asymptomatic women. The overall pooled HPV prevalence was 11% (95% confidence interval (CI), 9%-12%). The pooled HPV prevalence of 11% (95% CI, 9%-11%) was observed among women attending cervical cancer screening clinics. The pooled HPV prevalences were 10% (95% CI 8%-12%) and 11% (95% CI 4%-18%) from urban and rural areas respectively, indicating higher infection rates among the rural women with the least access to cancer screening and cancer care. Conclusion: The prevalence rates in this systematic quantitative review provide a reliable estimate of the burden of HPV infection among asymptomatic women from developed as well as developing nations. Rural women and women attending cervical cancer screening programmes feature higher genital HPV prevalences compared to their urban counterparts.