“…The study participants consisted of 511 women who were attended for diagnosis to a fertility clinic due to problems of achieving a clinical pregnancy after regular unprotected sexual intercourse (12 months or more). The study population at enrollment were in the reproductive age (between 25 and 39 years) [28].…”
Section: Study Populationmentioning
confidence: 99%
“…Urinary BPA concentrations were assessed utilizing validated gas chromatography ion-trap mass spectrometry [28]. The standard stock solutions (1 mg/mL) of BPA were prepared in acetonitrile.…”
Section: Sampling and Assessment Of Ovarian Reserve Parameters And Urinary Bpa Concentrationsmentioning
Background: Human exposure to environmentally widespread endocrine disruptors, especially bisphenol A (BPA), has been suggested to affect reproductive health. Animal studies indicate that BPA may play a role in the process of reproduction and impact on maturing oocytes, meiotic cell division or fertilization rate. Nevertheless, data regarding the effects of exposure to BPA on women’s ovarian function are still limited. Therefore, the aim of the current study is to assess the effects of environmental exposure to BPA on ovarian reserve. Methods: The study participants consisted of 511 women in reproductive age (25–39 years) who attended an infertility clinic for diagnosis, due to the couples’ infertility. BPA urinary concentrations were assessed by the validated gas chromatography ion-trap mass spectrometry method. The ovarian reserve was assessed using ovarian reserve parameters: Hormones concentrations: E2 (estradiol), FSH (follicle stimulating hormone), AMH (anti-Müllerian hormone), and AFC (antral follicle count). Results: In the present study, the negative association between BPA urinary concentrations and AMH (p = 0.02) and AFC (p = 0.03) levels was found. Exposure to BPA was not related to other examined parameters of ovarian reserve (FSH, E2). Conclusions: Our results suggest that BPA exposure may affect women ovarian reserve parameters and reduce ovarian reserve. As this is one of the first studies of its kind, the findings need confirmation in a further investigation.
“…The study participants consisted of 511 women who were attended for diagnosis to a fertility clinic due to problems of achieving a clinical pregnancy after regular unprotected sexual intercourse (12 months or more). The study population at enrollment were in the reproductive age (between 25 and 39 years) [28].…”
Section: Study Populationmentioning
confidence: 99%
“…Urinary BPA concentrations were assessed utilizing validated gas chromatography ion-trap mass spectrometry [28]. The standard stock solutions (1 mg/mL) of BPA were prepared in acetonitrile.…”
Section: Sampling and Assessment Of Ovarian Reserve Parameters And Urinary Bpa Concentrationsmentioning
Background: Human exposure to environmentally widespread endocrine disruptors, especially bisphenol A (BPA), has been suggested to affect reproductive health. Animal studies indicate that BPA may play a role in the process of reproduction and impact on maturing oocytes, meiotic cell division or fertilization rate. Nevertheless, data regarding the effects of exposure to BPA on women’s ovarian function are still limited. Therefore, the aim of the current study is to assess the effects of environmental exposure to BPA on ovarian reserve. Methods: The study participants consisted of 511 women in reproductive age (25–39 years) who attended an infertility clinic for diagnosis, due to the couples’ infertility. BPA urinary concentrations were assessed by the validated gas chromatography ion-trap mass spectrometry method. The ovarian reserve was assessed using ovarian reserve parameters: Hormones concentrations: E2 (estradiol), FSH (follicle stimulating hormone), AMH (anti-Müllerian hormone), and AFC (antral follicle count). Results: In the present study, the negative association between BPA urinary concentrations and AMH (p = 0.02) and AFC (p = 0.03) levels was found. Exposure to BPA was not related to other examined parameters of ovarian reserve (FSH, E2). Conclusions: Our results suggest that BPA exposure may affect women ovarian reserve parameters and reduce ovarian reserve. As this is one of the first studies of its kind, the findings need confirmation in a further investigation.
“…A handheld refractometer was used to assessed specific gravity (SG). The concentration of triclosan was measured using gas chromatography (Varian GC-450) coupled with tandem mass spectrometry (Varian 220-MS, ion-trap mass spectrometer as previously described (Jurewicz et al 2019)). External quality control was carried out by participation in the German External Quality Control Scheme (G-EQUAS), organized, and managed by the Institute and the Outpatient Clinic for Occupational, Social, and Environmental Medicine of the University of Erlangen-Nuremberg (Erlangen, Germany).…”
Section: Assessment Of Urinary Triclosan Concentrationsmentioning
Triclosan (TCS) is a widespread environmental endocrine-disrupting chemical. Animal and in vitro studies suggested that triclosan may affect homesostasis of sex and thyroid hormones and impact on reproduction. Due to limited data derived from human epidemiological studies, this study was performed to examine the association between urinary concentration of triclosan and in vitro reproductive outcomes (methaphase II (MII) oocyte yield, top quality embryo, fertilization rate, implantation rate, and clinical pregnancy) among women from infertility clinic. The study participants were enrolled in an Infertility Center in Poland. A total of 450 women aged 25–45 (n = 674 IVF cycles) provided urine samples. The urinary concentrations of triclosan were evaluated using validated gas chromatography ion-tap mass spectrometry method. Clinical outcomes of IVF treatment were abstracted from patients electronic chart records. Triclosan was detected in urine of 82% of women with geometric mean 2.56 ± 6.13 ng/mL. Urinary concentrations of triclosan were associated with decrease implantation rate (p = 0.03). There were no association between other examined IVF outcomes: MII oocytes, embryo quality, fertilization rate, and exposure to triclosan. As this is one of the first study on this topic, studies among larger and more diverse population are needed to confirm the results.
“…Triclosan (TCS) is recognized as a highly effective synthetic bacteriostatic agent. TCS is widely used in various fields, such as daily care products, agricultural production, food packaging materials, and medical products 1,2 . Worldwide, annual consumption of TCS is as high as 132 million liters 3 and the extensive application of TCS leads to its widespread presence in a variety of environmental media, thus causing serious water and soil pollution 4–7 .…”
Triclosan (TCS), a broad‐spectrum antimicrobial agent, is recognized as an environmental endocrine disruptor. TCS has caused a wide range of environmental, water and soil pollution. TCS is also still detected in food. Due to its high lipophilicity and stability, TCS can enter the human body through biological enrichment and potentially threatenes human health. In recent years, the neurotoxic effects caused by TCS contamination have attracted increasing attention. This study was designed to investigate the mechanism underlying TCS‐induced HT‐22 cells injury and to explore the effect of TCS on the PI3K/Akt, MAPK, and Nrf2/HO‐1 signaling pathways in HT‐22 cells. In this study, we examined the adverse effects of TCS treatment on ROS generation, and MDA, GSH‐Px, and SOD activities. The expression levels of proteins in the Nrf2, PI3K/Akt, MAPK pathways and Caspase‐3, BAX, Bcl‐2 were measured and quantified by Western blotting. The results showed that TCS could significantly reduce the activity of HT‐22 cells, increase the production of intracellular ROS and upregulate the expression of proapoptotic proteins. In addition, TCS promoted an increase in the MDA and SOD levels, and downregulated the GSH‐Px activity, and oxidative damage occurred in neurons. The mechanism underlying this toxicity was related to TCS‐induced PI3K/Akt/JNK‐mediated regulation of the Nrf2/HO‐1 signaling pathway. This result was further confirmed by the specific inhibitors LY294002 and SP600125. In summary, TCS could induce oxidative damage in HT‐22 neurons, and activation of the PI3K/Akt/JNK/ Nrf2 /HO‐1 signaling cascade was the main mechanism underlying the TCS‐induced HT‐22 neuronal toxicity.
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