Bisphenol A(BPA), BPS and BPB-induced oxidative stress and apoptosis mediated by mitochondria in human neuroblastoma cell lines

Wang, Congcong; He, Jinzhi; Xu, Tongfei; Han, Hongmei; Zhu, Zhaojie; Meng, Lingxue; Pang, Qihua; Fan, Ruifang

doi:10.1016/j.ecoenv.2020.111299

Cited by 86 publications

(41 citation statements)

References 69 publications

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“…In our previous studies, we found that ROS production played an important role in the BPA-induced apoptosis in IMR-32 and SK-N-SH cells by adding EGCG (an antioxidant) (Wang et al, 2021). We hypothesize that ROS also plays a similar role in the BPA-induced pyroptosis by detecting the expression levels of factors related to NLRP3/Caspase-1/GSDMD pathway after adding EGCG.…”

Section: Inhibition Of the Pyrotosis Of Imr-32 And Sk-n-sh Cells Exposed To Bpa By Egcgmentioning

confidence: 87%

“…Our previous study has shown that environmental BPA exposure can induce oxidative stress and mitochondrial apoptosis in different gender neuroblastoma cells (IMR-32 and SK-N-SH cells) (Wang et al, 2021). However, the mechanisms of the pyroptosis in IMR-32 and SK-N-SH cells exposed to low-dose BPA and the relationship between BPA exposure and apoptosis is not known.…”

Section: Introductionmentioning

confidence: 98%

“…For example, BPA exposure decreases the cognitive function, the ability of learning and memory and social response in rats (Negri-Cesi 2015; Zhang et al, 2019;Braun et al, 2017). Studies in the experimental models using primary hippocampus cells, HT-22 cell line and neuroblastoma cells have shown that low-dose BPA exposure induces oxidative stress and increases mitochondrial apoptosis (Meng et al, 2021;Wang et al, 2021;Pang et al, 2019). Epidemiological studies also show that BPA exposure during pregnancy or adolescence may cause neurobehavioral problems in childhood/adolescence (e.g., attention de cit hyperactivity disorder, depression, anxiety, autism spectrum disorders and social cognition/communication de cits) (Miodovnik et al, 2011;Perera et al, 2016;Li et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

Wang

Huang

et al. 2021

Preprint

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BackgroundBisphenol A (BPA) is an additive in polycarbonate and epoxy resin particles with endocrine disrupting effects. Previously it has been reported that BPA is neurotoxic via induction of cell apoptosis and inflammation, and our recent studies showed that even at nanomolar concentrations BPA accelerated the apoptosis and death of human neuroblastoma cells from both genders, whose mechanisms remain, however, unidentified.ResultsHuman neuroblastoma cell lines developed from male and female subjects, IMR-32 and SK-N-SH, respectively, were exposed to BPA at concentrations ranging from 1 nM to 100 μM, for 24 h, with or without epigallocatechin gallate (EGCG, 4 or 8 μM), Z-YVAD-FMK (1 or 10 μM, caspase-1 inhibitor), and ICI182.780 (100 nM or 3 μM, estrogen receptor inhibitor) as modulators. The results showed that BPA nonlinearly upregulated the levels of IL-18, ASC, GSDMD and NLRP3 mRNAs and that of NLRP3, caspase-1, GSDMD and IL-1β proteins in IMR-32 and SK-N-SH cells. Noticeably, the mRNA levels of caspase-1 and IL-1β were changed differently in the two cell lines: the level of caspase-1 mRNA was enhanced in IMR-32 cells but suppressed in SK-N-SH cells, and that of IL-1β was suppressed in IMR-32 cells but enhanced in SK-N-SH cells. The level of GSDMD expression in situ was along with the increase in the release of IL-1β, IL-18, caspase-1 and lactate dehydrogenase (LDH). Additionally, Z-YVAD-FMK, ICI182.780 and EGCG significantly reversed the changes of the above mRNAs/proteins induced by BPA. BPA significantly reduced the level of the reactive oxygen species and the rate of LDH leakage and apoptosis, while obviously increased the cell viability and the mitochondrial membrane potential. Meanwhile, Z-YVAD-FMK and ICI182.780 abruptly reduced the levels of Bak1, Bax, Bcl-2 and caspase-3 proteins induced by BPA. ConclusionAs mediated by the estrogen receptor, BPA may induce the pyroptosis of neuroblastoma cells through NLRP3/caspase-1/GSDMD signaling pathway, and caspase-1-dependent pyroptosis may be involved in BPA-induced apoptosis, which is alleviated by EGCG, an anti-oxidation agent.

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Section: Inhibition Of the Pyrotosis Of Imr-32 And Sk-n-sh Cells Exposed To Bpa By Egcgmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

Wang

Huang

et al. 2021

Preprint

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“…This regulation has forced producers to introduce BPA analogues like bisphenol S (BPS), bisphenol F (BPF), bisphenol E (BPE), and bisphenol B (BPB) to the market. These analogues can be found in environmental and biological samples and exhibit similar or even higher levels of toxicity [ 4 , 5 , 6 , 7 , 8 , 9 , 10 ]. For this reason, the EU has limited the SML for one of the BPA analogues (BPS) to 0.05 mg per kilogram of food [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Application of d-SPE before SPE and HPLC-FLD to Analyze Bisphenols in Human Breast Milk Samples

Tuzimski

Szubartowski

2021

Molecules

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In this study, we propose a simple, cost-effective, and sensitive high-performance liquid chromatography with fluorescence detection (HPLC-FLD) for the simultaneous determination of seven bisphenols (bisphenol F (BPF), bisphenol E (BPE), bisphenol B (BPB), BADGE (bisphenol A diglycidyl ether), BADGE∙2H2O, BADGE∙H2O, BADGE∙2HCl) in human breast milk samples. The dispersive solid phase extraction (d-SPE) coupled with solid phase extraction (SPE) procedure performed well for the majority of the analytes with recoveries in the range 57–88% and relative standard deviations (RSD%) of less than 9.4%. During the d-SPE stage, no significant matrix effect was observed thanks to the application of different pairs of salts such as zirconium-dioxide-based sorbents (Z-Sep or Z-Sep +) and primary secondary amine (PSA) or QuEChERS Enhanced Matrix Removal-Lipid (EMR-Lipid) and PSA. The method limits of quantification (mLOQs) for all investigated analytes were set at satisfactory low values in the range 171.89–235.11 ng mL−1. Analyte concentrations were determined as the average value from human breast milk matrix samples. The results show that the d-SPE/SPE procedure, especially with the application of EMR-Lipid and PSA, could be used for further bisphenol analyses in human breast milk samples.

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“…One of the outcomes of microglial activation (as well as that of macrophages, neutrophils, and endothelial cells) is the accumulation of reactive oxygen species (ROS) which include superoxide, singlet oxygen, hydroxyl radical, and hydrogen peroxide (H2O2). These molecules can damage proteins, DNA, and lipids at the cell membranes, ultimately leading to pathological changes of cell structure and function [27]. Mitochondria are the primary source of ROS in cells.…”

Section: Introductionmentioning

confidence: 99%

Ladostigil attenuates the oxidative and ER stress in human neuroblast-like SH-SY5Y cells

Zohar

Lezmi

Eliyahu

et al. 2021

Preprint

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A hallmark of the aging brain is the robust inflammation mediated by microglial activation. Neuroinflammation resulting from the induction of oxidative stress in neurodegenerative diseases and following brain injury. Chronic treatment of aging rats by ladostigil, a compound with antioxidant and anti-inflammatory function, prevented microglial activation and learning deficits. In this study, we investigate the effect of ladostigil on neuronal-like SH-SY5Y cells. We show that SH-SY5Y cells exposed to acute (by H2O2) or chronic oxidative stress (by Sin1, 3-morpholinosydnonimine) induced apoptotic cell death. However, in the presence of ladostigil, the decline in cell viability and the oxidative levels were partially reversed. RNA-seq analysis showed that chronic oxidation by Sin1 resulted in coordinated suppression of endoplasmic reticulum (ER) quality control and ER stress response gene sets. Chronic oxidative stress impacted ER proteostasis and induced the expression of numerous lncRNAs. Pre-incubation with ladostigil before exposing SH-SY5Y cells to Sin1 induced Clk1 (Cdc2-like kinase 1) which was implicated in psychophysiological stress in mice and Alzheimer disease. Ladostigil also suppressed the expression of Ccpg1 (Cell cycle progression 1) and Synj1 (Synaptojanin 1) that function in ER-autophagy and endocytic pathways. We postulate that ladostigil alleviated cell damage by oxidation and ER stress. Therefore, it may attenuate neurotoxicity and cell death that accompany chronic stress conditions in the aging brain.

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Bisphenol A(BPA), BPS and BPB-induced oxidative stress and apoptosis mediated by mitochondria in human neuroblastoma cell lines

Cited by 86 publications

References 69 publications

Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

Involvement of NLRP3/Caspase-1/GSDMD-Dependent Pyroptosis In BPA-Induced Apoptosis of Neuroblastoma Cells

Application of d-SPE before SPE and HPLC-FLD to Analyze Bisphenols in Human Breast Milk Samples

Ladostigil attenuates the oxidative and ER stress in human neuroblast-like SH-SY5Y cells

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