The genomic response of Ishikawa cells to bisphenol A exposure is dose- and time-dependent

Naciff, Jorge M.; Khambatta, Zubin S.; Reichling, T.; Carr, Gregory J.; Tiesman, Jay P.; Singleton, David W.; Khan, Sohaib A.; Daston, George P.

doi:10.1016/j.tox.2010.02.008

Cited by 54 publications

(34 citation statements)

References 36 publications

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“…These data are once again at odds with those of Aghajanova & Giudice (2011), who found altered levels of IGFBP1 but not of PRL. As discussed above, the incongruity between our results and those of Aghajanova & Giudice (2011) can be explained by the different BPA concentrations and exposure times used (Bredhult et al 2007, Naciff et al 2010.…”

Section: Effect Of Bpa On Secretion Of Biomarkers Of Endometrial Matucontrasting

confidence: 72%

“…The choice of short-term exposure (24 h) in the present study was guided by the report by Naciff et al (2010) who demonstrated that within this exposure time BPA is already able to alter the gene expression profile of Ishikawa cells. Taken together, the pieces of evidence that show an effect of 0.001 for all treatments vs control BPA on endometrial cell decidualization do raise concern, because altered transformation of the endometrium might contribute to reduced success of implantation (Singh et al 2011).…”

Section: Effect Of Bpa On Secretion Of Biomarkers Of Endometrial Matumentioning

confidence: 99%

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Bisphenol A modulates receptivity and secretory function of human decidual cells: an in vitro study

Mannelli¹,

Szóstek²,

Łukasik³

et al. 2015

Reproduction

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The human endometrium is a fertility-determining tissue and a target of steroid hormones' action. Endocrine disruptors (EDs) can exert adverse effects on the physiological function of the decidua at the maternal-fetal interface. We examined the potential effects of an ED, bisphenol A (BPA), on endometrial maturation/decidualization, receptivity, and secretion of decidual factors (biomarkers). In vitro decidualized, endometrial stromal cells from six hysterectomy specimens were treated with 1 pM-1 mM of BPA, for 24 h and assessed for cell viability and proliferation. Three non-toxic concentrations of BPA (1 mM, 1 nM, and 1 pM) were selected to study its influence on secretion of cell decidualization biomarkers (IGF-binding protein and decidual prolactin (dPRL)), macrophage migration inhibitory factor (MIF) secretion, and hormone receptors' expression (estrogen receptors (ERa and ERb); progesterone receptors (PRA and PRB); and human chorionic gonadotropin (hCG)/LH receptor (LH-R)). The results showed a decrease in cell viability (P!0.001) in response to BPA at the level of 1 mM. At the non-toxic concentrations used, BPA perturbed the expression of ERa, ERb, PRA, PRB, and hCG/LH-R (P!0.05). Furthermore, 1 mM of BPA reduced the mRNA transcription of dPRL (P!0.05). Secretion of MIF was stimulated by all BPA treatments, the lowest concentration (1 pM) being the most effective (P!0.001). The multi-targeted disruption of BPA on decidual cells, at concentrations commonly detected in the human population, raises great concern about the possible consequences of exposure to BPA on the function of decidua and thus its potential deleterious effect on pregnancy.Reproduction (2015) 150 115-125

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Section: Effect Of Bpa On Secretion Of Biomarkers Of Endometrial Matucontrasting

confidence: 72%

Section: Effect Of Bpa On Secretion Of Biomarkers Of Endometrial Matumentioning

confidence: 99%

Bisphenol A modulates receptivity and secretory function of human decidual cells: an in vitro study

Mannelli¹,

Szóstek²,

Łukasik³

et al. 2015

Reproduction

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“…This was evidenced by enhanced dendritic and synaptic development in cultured hypothalamic cells from fetal rats, as manifested by increases in the area of dot-like staining of synapsin I and MAP2-positive area (Iwakura et al 2010 ). Treatment of Ishikawa cell cultures with BPA also modulated the expression of the INSIG1 and FOS genes, which are implicated in regulating transcription and steroid metabolic processes, respectively (Naciff et al 2010 ).…”

Section: Effects Of In Utero Exposure To Bisphenol a On Male Reproducmentioning

confidence: 99%

Adverse Effects of Bisphenol A on Male Reproductive Function

Manfo

Jubendradass

Nantia

et al. 2013

Reviews of Environmental Contamination and Toxicology

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BPA is a ubiquitous environmental contaminant, resulting mainly from manufacturing,use or disposal of plastics of which it is a component, and the degradation of industrial plastic-related wastes. Growing evidence from research on laboratory animals, wildlife, and humans supports the view that BPA produces an endocrine disrupting effect and adversely affects male reproductive function. To better understand the adverse effects caused by exposure to BPA, we performed an up-to-date literature review on the topic, with particular emphasis on in utero exposure, and associated effects on spermatogenesis, steroidogenesis, and accessory organs.BPA studies on experimental animals show that effects are generally more detrimental during in utero exposure, a critical developmental stage for the embryo. BPA has been found to produce several defects in the embryo, such as feminization of male fetuses, atrophy of the testes and epididymides, increased prostate size, shortening of AGD, disruption of BTB, and alteration of adult sperm parameters (e.g.,sperm count, motility, and density). BPA also affects embryo thyroid development.During the postnatal and pubertal periods and adulthood, BPA affects the hypothalamic-pituitary-testicular axis by modulating hormone (e.g., LH and FSH,androgen and estrogen) synthesis, expression and function of respective receptors(ER, AR). These effects alter sperm parameters. BPA also induces oxidative stress in the testis and epididymis, by inhibiting antioxidant enzymes and stimulating lipid peroxidation. This suggests that employing antioxidants may be a promising strategy to relieve BPA-induced disturbances.Epidemiological studies have also provided data indicating that BPA alters male reproductive function in humans. These investigations revealed that men occupationally exposed to BPA had high blood/urinary BPA levels, and abnormal semen parameters. BPA-exposed men also showed reduced libido and erectile ejaculatory difficulties; moreover, the overall BPA effects on male reproduction appear to be more harmful if exposure occurs in utero. The regulation of BPA and BPA-related products should be reinforced, particularly where exposure during the fetal period can occur. The current TDI for BPA is proposed as 25 and 50 1-1g/kg bwt/day (European Food Safety Authority and Health Canada, respectively). Based on the evidence available, we believe that a TDI value of 5 1-1g/kg bwt/day is more appropriate (the endpoint is modulation of rat testicular function). Certain BPA derivatives are being considered as alternatives to BPA. However, certain of these related products display adverse effects that are similar to those of BPA. These effects should be carefully considered before using them as final alternatives to BPA in plastic production.

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“…The oestrogen responsiveness of cells was initially tested using EE 2 (Naciff et al 2010). A time-dependent increase in expression of both ESR2 and ESRRA target gene transcripts was seen (Fig.…”

Section: Time and Dose Responsiveness Of Esr2 And Esrra In Jurkat Cellsmentioning

confidence: 99%

Bisphenol A modulates the metabolic regulator oestrogen-related receptor-α in T-cells

Cipelli¹,

Harries²,

Okuda³

et al. 2014

Reproduction

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Bisphenol A (BPA) is a widely used plastics constituent that has been associated with endocrine, immune and metabolic effects. Evidence for how BPA exerts significant biological effects at chronic low levels of exposure has remained elusive. In adult men, exposure to BPA has been associated with higher expression of two nuclear receptors, oestrogen receptor-b (ERb) and oestrogen-related-receptor-a (ERRa), in peripheral white blood cells in vivo. In this study, we explore the expression of ESR2 (ERb) and ESRRA (ERRa) in human leukaemic T-cell lymphoblasts (Jurkat cells) exposed to BPA in vitro. We show that exposure to BPA led to enhanced expression of ESRRA within 6 h of exposure (meanGS.E.M.: 1.43G0.08-fold increase compared with the control, P!0.05). After 72 h, expression of ESRRA remained significantly enhanced at concentrations of BPA R1 nM. Oxidative metabolism of BPA by rat liver S9 fractions yields the potent oestrogenic metabolite, 4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP). Exposure of cells to 1-100 nM MBP increased the expression of both ESRRA (significantly induced, P!0.05, at 1, 10, 100 nM) and ESR2 (1.32G0.07-fold increase at 100 nM exposure, P!0.01). ERRa is a major control point for oxidative metabolism in many cell types, including T-cells. Following exposure to both BPA and MBP, we found that cells showed a decrease in cell proliferation rate. Taken together, these results confirm the bioactivity of BPA against putative T-cell targets in vitro at concentrations relevant to general human exposure.

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The genomic response of Ishikawa cells to bisphenol A exposure is dose- and time-dependent

Cited by 54 publications

References 36 publications

Bisphenol A modulates receptivity and secretory function of human decidual cells: an in vitro study

Bisphenol A modulates receptivity and secretory function of human decidual cells: an in vitro study

Adverse Effects of Bisphenol A on Male Reproductive Function

Bisphenol A modulates the metabolic regulator oestrogen-related receptor-α in T-cells

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