Probiotic Administration Mitigates Bisphenol A Reproductive Toxicity in Zebrafish

Although the use of bisphenol A (BPA) has been banned in a number of countries, its presence in the environment still creates health issues both for humans and wildlife. So far, BPA toxicity has been largely investigated on different biological processes, from reproduction to development, immune system, and metabolism. In zebrafish, Danio rerio, previous studies revealed the ability of environmentally relevant concentrations of this contaminant to significantly impair fertility via epigenetic modification. In addition, several studies demonstrated the ability of different probiotic strains to improve organism health. This study provides information on the role of the probiotic mixture SLAb51 to counteract adverse BPA effects on reproduction. A 28-day trial was set up with different experimental groups: BPA, exposed to 10 µg/L BPA; P, receiving a dietary supplementation of SLAb51 at a final concentration of 109 CFU/g; BPA+P exposed to 10 µg/L BPA and receiving SLAb51 at a final concentration of 109 CFU/g and a C group. Since oocyte growth and maturation represent key aspects for fertility in females, studies were performed on isolated class III (vitellogenic) and IV (in maturation) follicles and liver, with emphasis on the modulation of the different vitellogenin isoforms. In males, key signals regulating spermatogenesis were investigated. Results demonstrated that in fish exposed to the combination of BPA and probiotic, most of the transcripts were closer to C or P levels, supporting the hypothesis of SLAb51 to antagonize BPA toxicity. This study represents the first evidence related to the use of SLAb51 to improve reproduction and open new fields of investigation regarding its use to reduce endocrine disrupting compound impacts on health.

Benzo[a]pyrene impairs the migratory pattern of human gonadotropin-releasing-hormone-secreting neuroblasts

Benzo[a]pyrene (BaP) is a widespread pollutant that can act as an endocrine disrupting compound (EDC) and interferes with reproductive function. The central regulatory network of the reproductive system is mediated by gonadotropin-releasing hormone (GnRH) neurons, which originate in the olfactory placode and, during ontogenesis, migrate into the hypothalamus. Given the importance of the migratory process for GnRH neuron maturation, we investigated the effect of BaP (10 µM for 24 h) on GnRH neuroblasts isolated from the human fetal olfactory epithelium (FNCB4). BaP exposure significantly reduced the mRNA level of genes implicated in FNCB4 cell migration and affected their migratory ability. Our findings demonstrate that BaP may interfere with the central neuronal network controlling human reproduction affecting GnRH neuron maturation.

Acute Exposure to Bisphenol A Causes Oxidative Stress Induction with Mitochondrial Origin in Saccharomyces cerevisiae Cells

Bisphenol A (BPA) is a major component of the most commonly used plastic products, such as disposable plastics, Tetra Paks, cans, sport protective equipment, or medical devices. Due to the accumulation of excessive amounts of plastic waste and the subsequent release of BPA into the environment, BPA is classified as a pollutant that is undesirable in the environment. To date, the most interesting finding is the ability of BPA to act as an endocrine disrupting compound due to its binding to estrogen receptors (ERs), and adverse physiological effects on living organisms may result from this action. Since evidence of the potential pro-oxidizing effects of BPA has accumulated over the last years, herein, we focus on the detection of oxidative stress and its origin following BPA exposure using pulsed-field gel electrophoresis, flow cytometry, fluorescent microscopy, and Western blot analysis. Saccharomyces cerevisiae cells served as a model system, as these cells lack ERs allowing us to dissect the ER-dependent and -independent effects of BPA. Our data show that high concentrations of BPA affect cell survival and cause increased intracellular oxidation in yeast, which is primarily generated in the mitochondrion. However, an acute BPA exposure does not lead to significant oxidative damage to DNA or proteins.

Increased PACAP- and DβH-Positive Hepatic Nerve Fibers after Bisphenol A Exposure

Bisphenol A (BPA) is an endocrine-disrupting compound (EDC) that can be found nearly everywhere in our polluted world. BPA has been correlated with pathophysiologies that include psychological disorders, especially in children. This study used juvenile porcine models to investigate the effects of BPA on the liver of developing vertebrates in order to determine the effects of BPA on innervated hepatic samples with the use of double-labeled immunofluorescence. This study specifically investigated the sympathetic nervous system (SNS) colocalized with a specific neural marker (PACAP) that has previously been correlated with specific pathophysiologies in the literature. In the liver, it was observed that there were significantly increased nerve fibers in the SNS colocalized with the neural marker PACAP after exposure to BPA at concentrations considered to be “safe” with the same or more profound effects at higher exposure levels. The implications of childhood exposure to BPA are then discussed with regard to several correlation studies that have linked BPA exposure to behavioral/psychological disorders. It is possible that BPA exposure in childhood may upregulate the SNS and PACAP levels, thereby contributing to the correlations in the literature.

Facile Synthesis of Porous ZnO Nanoparticles Efficient for Photocatalytic Degradation of Biomass-Derived Bisphenol A Under Simulated Sunlight Irradiation

Bisphenol A (BPA) produced from biomass is a typical endocrine disrupting compound that is carcinogenic and genotoxic and can be accumulated in water due to its extensive use and difficult degradation. In this study, the porous ZnO photocatalyst with core-shell structure and large surface area was successfully developed for the efficient photocatalytic degradation of BPA. The various effects of calcination temperatures, BPA concentrations, ZnO dosages, pH and inorganic ions on the degradation performance were systemically studied. The results showed that 99% degradation of BPA was achieved in 1 h using the porous ZnO calcined at 550°C under the conditions of 30 mg/L BPA, 1 g/L ZnO, and pH of 6.5. Besides, the inhibition effects of anions for the photocatalytic removal of BPA decreased in the order of H2PO4- > HCO3- > SO42- > Cl−, while the cations K+, Ca2+, and Na+ had little effect on the photocatalytic degradation of BPA. The results of scavenging experiments showed that h+, ·O2-, and e− played the key role in the photocatalytic degradation process. Finally, the main pathways of BPA degradation were proposed based on ten intermediates found in the degradation process. This work may provide a good guideline to degrade various endocrine disrupting compounds in wastewater treatment.

Oxidative Stress and Apoptosis Contributed to Nonylphenol-Induced Cell Damage in Mouse NCTC Clone 1469 Cells

Nonylphenol (NP) is considered an environmental toxicant and endocrine-disrupting compound. The present study aimed to investigate the effects of NP on NCTC Clone 1469, nonparenchymal hepatocytes, and to study the molecular basis of NP-induced liver injury. The results showed that NP decreased cell viability and induced nucleus crenulation and intracellular enzyme leakage in NCTC Clone 1469 cells. Additionally, NP-induced oxidative stress and apoptosis of NCTC Clone 1469 are accompanied by upregulating reactive oxygen species (ROS) production, increase of Bax, decrease of Bcl-2, activation of caspase-3 and caspase-12, and release of cytosolic free Ca2+ in the cells. ROS scavenger, N-acetyl-L-cysteine (NAC), prevented the intracellular enzyme leakage induced by NP. NP induced alteration of estrogen receptor- (ER-) α and ER-β expression, while ER antagonists, ICI 182,780, showed no effect on NP-induced intracellular enzyme leakage. We proposed that NP triggered cell damage via inducing oxidative stress and apoptosis in cells, but not estrogenic effect.

Bisphenol A as a risk factor for allergic rhinitis in children

Aim: Bisphenol-A (BPA) is an endocrine disrupting compound and may exacerbate or induce allergic diseases. To the best of our knowledge, there is little evidence regarding the effects of BPA exposure on allergic rhinitis (AR) in children. In the present study, we sought to examine whether exposure to BPA in children is associated with AR. Methods: This study was designed as a case controlled clinical study. 140 children diagnosed as allergic rhinitis and 140 healthy children as control group were recruited. BPA, interleukin-4, interleukin-13, total IgE and interferon-gamma levels were determined. Skin prick tests were performed in patient group. Total nasal symptom score and ARIA classification were used to predict disease severity. Results: Serum IL-4, IgE and BPA levels of children with allergic rhinitis were found to be significantly higher than the control group. BPA and IL-4 levels were significantly higher in moderate to severe-persistent group. There was a positive correlation between total nasal symptom scores and Bisphenol A levels in children with allergic rhinitis. Conclusions: The present study is the first to observe statistically significant relationship between BPA concentrations and allergic rhinitis in children. Also increased levels of BPA are associated with disease severity.

Basic Fibroblast Growth Factor is Involved in Bisphenol S Induced Proliferation of Hemangioma Cells

BackgroundThe hyperproliferation of mesoblastic vascular tissues can lead to the incidence of hemangioma (IHA), which is the most common benign tumor in infants. Estrogenic signals can trigger the progression of HA via activation of gene transcription.ResultsWe found that bisphenol S (BPS), one widely spread endocrine disrupting compound (EDC), can induce the proliferation of HA cells and trigger the G1 to S transition of cell cycle. Among the tested cytokines, BPS can up regulate of basic fibroblast growth factor (bFGF). Targeted inhibition of bFGF via its neutralization antibody can reverse BPS induced cell proliferation. Mechanistically, BPS can increase the mRNA expression of bFGF via increasing the transcription and mRNA stability. The activation of p65 and down regulation of miR-155-5p were responsible for BPS induced transcription and mRNA stability of bFGF, respectively. Conclusions: BPS can increase the expression of bFGF via activation of p65 and down regulation of miR-155-5p, which resulted in the proliferation of HA cells.