scholarly journals Endocrine disrupting chemical, bisphenol-A, induces breast cancer associated gene HOXB9 expression in vitro and in vivo

Gene ◽  
2016 ◽  
Vol 590 (2) ◽  
pp. 234-243 ◽  
Author(s):  
Paromita Deb ◽  
Arunoday Bhan ◽  
Imran Hussain ◽  
Khairul I. Ansari ◽  
Samara A. Bobzean ◽  
...  
2020 ◽  
Vol 2 (4) ◽  
pp. 89-94
Author(s):  
Nikola Knizatova ◽  
Katarína Tokárová ◽  
Hana Greifová ◽  
Tomáš Jambor ◽  
Peter Massányi ◽  
...  

Bisphenol A (BPA) is the most well-known compound from the bisphenol family. There is increasing evidence that bisphenol BPA used in plastics, receipts, food packaging, and other products might be harmful to human health due to its actions as an endocrine-disrupting chemical, therefore BPA is being replaced by compounds very similar in structure, but data on the occurrence and effects of these BPA analogs are limited. Therefore, there is increasing concern regarding human exposure to bisphenol analogs (BPs) due to their widespread use and potential adverse effects. The main objective of this work was to investigate human exposure to BPs and the associated endocrine activities. We performed a literature review of the available research made in humans, in in vivo and in vitro tests. The findings support the idea that exposure to BPs may have an impact on human health, especially in terms of endocrine disruption.


Author(s):  
Aylin Jamali Khaghani ◽  
Parisa Farrokh ◽  
Saeed Zavareh

Background: Bisphenol A (BPA), a synthetic endocrine-disrupting chemical, is a reproductive toxicant. Granulosa cells have significant roles in follicle development, and KIT ligand (KITL) and Anti-Müllerian hormone (AMH) are essential biomolecules produced by them during folliculogenesis. Objective: Due to the widespread use of BPA and its potential epigenetic effects, this study examined the impact of BPA on promoter methylation of amh and kitl genes in mouse granulosa cells. Materials and Methods: Preantral follicles were isolated from ovaries of immature mice and cultured for eight days. Then, follicles were treated with 50 and 100 μM of BPA, and 0.01% (v/v) ethanol for 24 and 72 hr. Growth and degeneration of follicles and antrum formation were analyzed. The granulosa cells were isolated mechanically, and their extracted DNA was treated with sodium bisulfite. The promoter regions of the amh and kitl were analyzed with PCR and sequencing. Results: BPA did not change follicle survival and antrum formation significantly (p = 0.41). However, the culture in the presence of 100 μM BPA had an inhibitory effect on growth. Before BPA treatment, the CpG of the kitl and amh promoters were unmethylated and partially methylated, respectively. While the percent of 5mC in the amh promoter reduced at 100 μM of BPA, it did not alter the kitl promoter methylation. Conclusion: BPA at higher concentrations has an inhibitory effect on follicle growth. Moreover, it seems that the epigenetic impact of BPA restricts to the demethylation of CpG sites. Key words: Bisphenol A, DNA methylation, Granulosa cells.


2019 ◽  
Vol 35 (4) ◽  
pp. 294-303 ◽  
Author(s):  
Asad Ullah ◽  
Madeeha Pirzada ◽  
Sarwat Jahan ◽  
Hizb Ullah ◽  
Muhammad Jamil Khan

Bisphenol A (BPA) is a well-known endocrine-disrupting chemical with estrogenic activity. The widespread exposure of individuals to BPA is suspected to affect a variety of physiological functions, including reproduction, development, and metabolism. Here we report the mechanisms by which BPA and three of its analogues bisphenol B (BPB), bisphenol F (BPF), and bisphenol S (BPS) cause generation of reactive oxygen species (ROS), sperm DNA damage, and oxidative stress in both in vivo and in vitro rat models. Sperm were incubated with different concentrations (1, 10, and 100 µg/L) of BPA and its analogues BPB, BPF, and BPS for 2 h. BPA and its analogues were observed to increase DNA fragmentation, formation of ROS, and affected levels of superoxide dismutase at higher concentration groups. In an in vivo experiment, rats were exposed to different concentrations (5, 25, and 50 mg/kg/day) of BPA, BPB, BPF, and BPS for 28 days. In the higher dose (50 mg/kg/day) treated groups of BPA and its analogues BPB, BPF, and BPS, DNA damage was observed while the motility of sperm was not affected.


2019 ◽  
Author(s):  
Sophie-Christine de Aguiar Greca ◽  
Ioannis Kyrou ◽  
Ryan Pink ◽  
Harpal Randeva ◽  
Dimitris Grammatopoulos ◽  
...  

2020 ◽  
Vol 9 (2) ◽  
pp. 405 ◽  
Author(s):  
Sophie-Christine de Aguiar Greca ◽  
Ioannis Kyrou ◽  
Ryan Pink ◽  
Harpal Randeva ◽  
Dimitris Grammatopoulos ◽  
...  

Background: Endocrine-disrupting chemicals (EDCs) are environmental chemicals/toxicants that humans are exposed to, interfering with the action of multiple hormones. Bisphenol A (BPA) is classified as an EDC with xenoestrogenic activity with potentially adverse effects in reproduction. Currently, a significant knowledge gap remains regarding the complete spectrum of BPA-induced effects on the human placenta. As such, the present study examined the effects of physiologically relevant doses of BPA in vitro. Methods: qRT-PCR, Western blotting, immunofluorescence, ELISA, microarray analyses, and bioinformatics have been employed to study the effects of BPA using nonsyncytialised (non-ST) and syncytialised (ST) BeWo cells. Results: Treatment with 3 nM BPA led to an increase in cell number and altered the phosphorylation status of p38, an effect mediated primarily via the membrane-bound estrogen receptor (GPR30). Nonbiased microarray analysis identified 1195 and 477 genes that were differentially regulated in non-ST BeWo cells, whereas in ST BeWo cells, 309 and 158 genes had altered expression when treated with 3 and 10 nM, respectively. Enriched pathway analyses in non-ST BeWo identified a leptin and insulin overlap (3 nM), methylation pathways (10 nM), and differentiation of white and brown adipocytes (common). In the ST model, most significantly enriched were the nuclear factor erythroid 2-related factor 2 (NRF2) pathway (3 nM) and mir-124 predicted interactions with cell cycle and differentiation (10 nM). Conclusion: Collectively, our data offer a new insight regarding BPA effects at the placental level, and provide a potential link with metabolic changes that can have an impact on the developing fetus.


2003 ◽  
Vol 31 (3) ◽  
pp. 551-561 ◽  
Author(s):  
H Inoshita ◽  
H Masuyama ◽  
Y Hiramatsu

An endocrine-disrupting chemical (EDC) can alter endocrine functions through a variety of mechanisms, including nuclear receptor-mediated changes in protein synthesis, interference with membrane receptor binding, steroidogenesis or synthesis of other hormones. Although major chemicals have been shown to disrupt estrogenic actions mainly through their binding to estrogen receptor (ER) or androgen receptor, it is not clear how EDCs affect endocrine functions in vivo. We present evidence that the EDCs bisphenol A and phthalate activate ER-mediated transcription through interaction with TRAP220. Moreover, bisphenol A had positive effects on the interaction between ER-beta and TRAP220 and on the expression of ER-beta and TRAP220 compared with phthalate and estradiol in uterine tIssue. These data suggested that some EDCs might alter endocrine function through the change of the receptor and coactivator levels in uterine tIssue and through the different effect on the interaction between ERs and coactivator TRAP220.


Author(s):  
Arunoday Bhan ◽  
Imran Hussain ◽  
Khairul I. Ansari ◽  
Samara A.M. Bobzean ◽  
Linda I. Perrotti ◽  
...  

2020 ◽  
Vol 89 (3) ◽  
pp. e441
Author(s):  
Justyna Milczarek-Banach ◽  
Piotr Miśkiewicz

Bisphenols (BPs) are common plastic additives widely used in industry, hence, human exposure to BPs is inevitable. The best known BP is bisphenol A (BPA), the production of which and its analogues has been increasing worldwide. This chemical is classified as an endocrine-disrupting chemical, inferring with hormonal homeostasis. Indeed, BPA is associated with the development of oestrogen-dependent neoplasms, infertility, metabolic disorders and neurobehavioral disturbances. However, there is a lack of evidence regarding the impact of BPA and its analogues on the thyroid, with most studies mainly performed on animals or in vitro. This review aims to summarise the knowledge regarding the relationship between BPA and its analogues on the thyroid gland.


2015 ◽  
Vol 54 (3) ◽  
pp. 289-303 ◽  
Author(s):  
Ciro Menale ◽  
Maria Teresa Piccolo ◽  
Grazia Cirillo ◽  
Raffaele A Calogero ◽  
Alfonso Papparella ◽  
...  

Bisphenol A (BPA) is a xenobiotic endocrine-disrupting chemical.In vitroandin vivostudies have indicated that BPA alters endocrine-metabolic pathways in adipose tissue, which increases the risk of metabolic disorders and obesity. BPA can affect adipose tissue and increase fat cell numbers or sizes by regulating the expression of the genes that are directly involved in metabolic homeostasis and obesity. Several studies performed in animal models have accounted for an obesogen role of BPA, but its effects on human adipocytes – especially in children – have been poorly investigated. The aim of this study is to understand the molecular mechanisms by which environmentally relevant doses of BPA can interfere with the canonical endocrine function that regulates metabolism in mature human adipocytes from prepubertal, non-obese children. BPA can act as an estrogen agonist or antagonist depending on the physiological context. To identify the molecular signatures associated with metabolism, transcriptional modifications of mature adipocytes from prepubertal children exposed to estrogen were evaluated by means of microarray analysis. The analysis of deregulated genes associated with metabolic disorders allowed us to identify a small group of genes that are expressed in an opposite manner from that of adipocytes treated with BPA. In particular, we found that BPA increases the expression of pro-inflammatory cytokines and the expression ofFABP4andCD36, two genes involved in lipid metabolism. In addition, BPA decreases the expression ofPCSK1, a gene involved in insulin production. These results indicate that exposure to BPA may be an important risk factor for developing metabolic disorders that are involved in childhood metabolism dysregulation.


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