Biological effects of chronic and acute exposure of human endothelial cell line EA.hy926 to bisphenol A: New tricks from an old dog

Kokai, Dunja; Stanić, Bojana; Nenadov, Dragana Samardzija; Pogrmić-Majkić, Kristina; Tesic, Biljana; Fa, Svetlana; Andrić, Nebojša

doi:10.1016/j.chemosphere.2020.127159

Cited by 18 publications

(6 citation statements)

References 58 publications

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“…However, excessive production of NO can interact with proteins, fats, nucleic acids and other biomolecules in the organisms, resulting in toxic damage to the organisms 53,54 . BPA can induce NO production and cause damage to the organism, for example, BPA increased NO production in EA.hy926 cells and induced functional and molecular changes associated with the promotion of endothelial integrity through activation of the ER/Akt/eNOS pathways 49 . Furthermore, BPA intensified NO production and caused sex‐dependent dysregulation of human neutrophil responses, 55 and BPA induced neurotoxicity effects in human embryonic stem cells via production of RNS mediated by iNOS and nNOS 56 .…”

Section: Discussionmentioning

confidence: 99%

“…42 Se deficiency is a predisposing condition that enhances vulnerability to various toxicants, pathogens, and degenerative disorders, 43 and it has impaired various tissues and cells, 44 including liver, 45 spleen 46 and intestinal porcine jejunal epithelial cells, 47 especially the kidney owes to it being a target organ for Se deficiency. 48 Researchers have found that BPA exposure potentially increases NO levels, 49 and NO could regulate the AMPK/mTOR signaling pathways to contribute to the autophagy. [16][17][18] In the present study, we found that BPA exposure increased NO levels and iNOS activity, activated AMPK/mTOR signaling pathways, and stimulated p62/LC3/Beclin1 signaling, resulting in As an important biological messenger, NO is involved in various defense mechanisms of the organisms, including anti-infection, 50 antiinflammation 51 and anti-tumor.…”

Section: Discussionmentioning

confidence: 99%

“…53,54 BPA can induce NO production and cause damage to the organism, for example, BPA increased NO production in EA.hy926 cells and induced functional and molecular changes associated with the promotion of endothelial integrity through activation of the ER/Akt/ eNOS pathways. 49 Furthermore, BPA intensified NO production and caused sex-dependent dysregulation of human neutrophil responses, 55 and BPA induced neurotoxicity effects in human embryonic stem cells via production of RNS mediated by iNOS and nNOS. 56 Similarly, we observed that NO and iNOS levels in the BPA group were significantly induced, indicating that excessive NO occurred during BPA exposure in the chicken kidney.…”

Section: Discussionmentioning

confidence: 99%

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Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

Chen

Zhang

et al. 2022

Environmental Toxicology

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Bisphenol A (BPA), a phenolic compound, is harmful to humans and animals as its residue in the water threatens multiple organs, especially the kidney. Low selenium (Se) diets are consumed in many regions of the world, and poor Se status has exacerbating effect on toxicity of several environmental chemicals. Here, we described the discovery path of Se deficiency aggravation on autophagy in BPA treated chicken kidney through regulating nitric oxide (NO) and adenosine monophosphate activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathways.The actual dietary Se intake for chickens was 0.30 mg/kg in control group and 0.03 mg/kg in Low-Se group, and BPA exposure concentration for chickens was 0.05 g/kg. Chicken embryo kidney (CEK) cells were used in vitro and the BPA exposure concentration for CEK cells was 150 nM. We found that BPA significantly increased levels of NO and inducible nitric oxide synthase, activated AMPK/mTOR signaling pathways, thereby triggering p62/LC3/Beclin1 signaling, resulting in formations of autophagosome and autolysosome, and finally stimulating autophagy in the chicken kidney. Additionally, Se deficiency promoted the occurrence of autophagy in BPA-treated kidneys. Altogether, our findings showed that Se deficiency exacerbates BPA-induced renal autophagy in chickens via regulation of NO and AMPK/mTOR signaling pathways. These findings will improve our understandings of the mechanisms of nephrotoxicity of BPA and detoxification by Se in chickens. In addition, further work is required to determine if Se status of exposed populations needs to be considered in future epidemiological assessments.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

Chen

Zhang

et al. 2022

Environmental Toxicology

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“…To gain insight into the long-term effects of EDs in human cells, a limited number of studies employed immortalized cell lines that may be exposed to EDs for longer periods of time. Some of these studies revealed a distinct effect on steroidogenesis following a long-term exposure of human granulosa cells to the mixture of EDs [ 14 ], an ED-specific transcriptional reprograming in human breast cancer cells [ 15 ], dynamic, time-dependent changes in the response of human bronchial epithelial cells to the total particulate matter from a candidate modified-risk tobacco product [ 16 ], or a specific bisphenol-A-mediated effect in human vascular endothelial cells [ 17 ]. Moreover, long-term exposure studies also help in better understanding the biological effects of the relevant levels of several EDs in trophoblasts [ 18 ] or the molecular events involved in malignant transformation [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of In Vitro Long-Term Low-Level DEHP Exposure on Gene Expression Profile in Human Granulosa Cells

Nenadov

Pogrmić-Majkić

Tesic

et al. 2022

Cells

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Here, we applied a model of long-term exposure of human granulosa cells to low environmentally relevant levels of di(2-ethylhexyl) phthalate (DEHP). This approach provides more relevant data regarding the impact of DEHP on the function of human granulosa cells. The immortalized human granulosa cells HGrC1 were exposed to 50 nM and 250 nM DEHP for four weeks. The cells were collected every week to analyze the basal granulosa cells’ functions. A portion of the DEHP-exposed cells was stimulated with forskolin (FOR) for 48 h. Steroidogenesis was investigated using ELISA, whereas DNBQ sequencing and RT-qPCR were used to analyze gene expression. The results show that steroidogenesis was not affected by DEHP exposure. RNAsequencing shows that DEHP caused week- and concentration-specific changes in various genes and functions in HGrC1. Sulfotransferase family 1A member 3 (SULT1A3) and 4 (SULT1A4), which are involved in catecholamine metabolism, were the most prominent genes affected by DEHP under both the basal and FOR-stimulated conditions in all four weeks of exposure. This study showed, for the first time, that SULT1A3 and SULT1A4 are expressed in human granulosa cells, are regulated by FOR, and are affected by low-level DEHP exposure. These data provide new insight into the relationship between DEHP, SULT1A3, and SULT1A4 in human granulosa cells.

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“…An increasing number of studies have revealed widespread exposure and its adverse effects. Animal toxicology studies and epidemiologic studies have shown effects of perinatal and postnatal BPA exposure on metabolic disorders and reproductive and developmental abnormalities of the offspring. − These effects caused by BPA often occur at concentrations below the recommended safe daily exposure level. It is widely controversial that the utility of current guideline studies for evaluating the safety of BPA .…”

Section: Introductionmentioning

confidence: 99%

Bisphenol Analogues and Their Chlorinated Derivatives in Breast Milk in China: Occurrence and Exposure Assessment

Niu

Wang

Yang

et al. 2021

J. Agric. Food Chem.

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Concentrations of bisphenol A (BPA) and its analogues (together with their chlorinated derivatives are referred to as BPs) were measured in 181 breastmilk samples collected from 9 provinces in China in 2014. Twelve BP types were found. The BP concentrations ranged from not detected to 5.912 μg/L. BPA was the predominant BP, followed by bisphenol F (BPF) and bisphenol S (BPS). The mean BPA, BPF, and BPS levels were 0.444, 0.107, and 0.027 μg/L, respectively. Other BPs were sporadically detected in breastmilk samples. There were no differences (p > 0.05) in BPA, BPF, BPS, or total BP levels in the urban and rural regions or the northern and southern regions. BPA accounted for approximately 70% of the BPs and BPF accounted for more than 20% of the BPs in breast milk samples. The high contribution of BPF indicated that BPA analogues, not only BPA, should receive attention. The upper-bound daily intakes of BPs for infants 0–6 months old were 0.044–1.291 μg/kg bw/day. Despite the absence of tolerable daily intake data, attention should be paid not only on BPA but also BPF.

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Biological effects of chronic and acute exposure of human endothelial cell line EA.hy926 to bisphenol A: New tricks from an old dog

Cited by 18 publications

References 58 publications

Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

Impact of In Vitro Long-Term Low-Level DEHP Exposure on Gene Expression Profile in Human Granulosa Cells

Bisphenol Analogues and Their Chlorinated Derivatives in Breast Milk in China: Occurrence and Exposure Assessment

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