Effect of estradiol and bisphenol A on human hepatoblastoma cell viability and telomerase activity

Xu, Binghe; Zhao, Qi; Gao, Xiaohua; Hou, Guangjun

doi:10.1590/1414-431x20154400

Cited by 5 publications

(3 citation statements)

References 22 publications

(23 reference statements)

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“…BPA functions mainly by mimicking the activity of oestrogen hormone. Correlations between oestrogen and tumors have been well established and research suggests that oestrogen promotes angiogenesis as well 11 . BPA in liver gets metabolized and enters the blood circulation and finally gets excreted with urine.…”

Section: Resultsmentioning

confidence: 99%

Untitled

2018

IJPSR

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Bisphenol A (BPA) is primarily used in the manufacture of plastics and resins. There are many scientific reports that point to the adverse effects of this chemical to different animal models. There has been an increase in use of plastic during the last couple of decades and this has increased human exposure to plasticizers like Bisphenol A. But since little is known on how these endocrine disruptors especially BPA promote cancer progression, the study investigated the effect of BPA on hepatocellular carcinoma cell line Hep-G2 by evaluating the expression of molecules involved in the processes of inflammation, cancer and angiogenesis. Cell viability studies using MTT assay, RT-PCR studies and Western blotting studies were performed to check effect of Bisphenol A on liver cancer cells. Cell viability studies, RT-PCR studies and Western blotting studies showed a dose dependent increase in the expression of factors involved in cancer progression which decreased when the cells were treated with Meloxicam, a COX-2 inhibitor. The results indicate that BPA up-regulates the expression of factors involved in the inflammatory pathway thus helping in the progression of cancer.

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Section: Resultsmentioning

confidence: 99%

Untitled

2018

IJPSR

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“…Several studies have reported that BPA and E2 are acting the same way in vitro . For instance, BPA and E2 were both shown to promote HepG2 cell proliferation by inhibition of apoptosis and stimulation of telomerase activity via an estrogen receptor-dependent pathway ( 43 ). In our study, metabolomics revealed modulations of the HepG2 metabolome that are molecule specific (discrimination between the BPA exposed groups and the E2 exposed group).…”

Section: Discussionmentioning

confidence: 99%

An Untargeted Metabolomics Approach to Investigate the Metabolic Modulations of HepG2 Cells Exposed to Low Doses of Bisphenol A and 17β-Estradiol

et al. 2018

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The model xeno-estrogen bisphenol A (BPA) has been extensively studied over the past two decades, contributing to major advances in the field of endocrine disrupting chemicals research. Besides its well documented adverse effects on reproduction and development observed in rodents, latest studies strongly suggest that BPA disrupts several endogenous metabolic pathways, with suspected steatogenic and obesogenic effects. BPA's adverse effects on reproduction are attributed to its ability to activate estrogen receptors (ERs), but its effects on metabolism and its mechanism(s) of action at low doses are so far only marginally understood. Metabolomics based approaches are increasingly used in toxicology to investigate the biological changes induced by model toxicants and chemical mixtures, to identify markers of toxicity and biological effects. In this study, we used proton nuclear magnetic resonance (1H-NMR) based untargeted metabolite profiling, followed by multivariate statistics and computational analysis of metabolic networks to examine the metabolic modulation induced in human hepatic cells (HepG2) by an exposure to low and very low doses of BPA (10−6M, 10−9M, and 10−12M), vs. the female reference hormone 17β-estradiol (E2, 10−9M, 10−12M, and 10−15M). Metabolomic analysis combined to metabolic network reconstruction highlighted different mechanisms at lower doses of exposure. At the highest dose, our results evidence that BPA shares with E2 the capability to modulate several major metabolic routes that ensure cellular functions and detoxification processes, although the effects of the model xeno-estrogen and of the natural hormone can still be distinguished.

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“…Кроме того, представлены данные о влиянии БФА непосредственно на экспрессию генов -рецепторов гормонов, в частности эстрогенов. Например, это было показано в культуре клеток мозжечка крысы и нейро бластомы человека, а также на клеточных линиях человека H295R (кора надпочечников, ангиотензин-II-чувствительная, стероид-продуцирующая линия), HEK293 (клетки почки эмбриона), HepG2 (карцинома печени) [65][66][67].…”

Section: механизмы действия бисфенола а как вещества разрушающего эндокринную системуunclassified