Bisphenol A and several derivatives exert neural toxicity in human neuron-like cells by decreasing neurite length

Liang, Xiaoxing; Yin, Nuoya; Liang, Shengxian; Yang, Renjun; Liu, Shu-Yu; Lu, Yuanping; Jiang, Linshu; Zhou, Qunfang; Jiang, Guibin; Faiola, Francesco

doi:10.1016/j.fct.2019.111015

Cited by 42 publications

(21 citation statements)

References 39 publications

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“…It is considered to affect important signaling pathways via ER or kinase signaling receptors, leading to abnormalities in neural development (Ge et al, 2014;Baba et al, 2009). BPA has been shown to attenuate neurite extension (Seki et al, 2011;Liang et al, 2020), branching (Wu et al, 2016), neuron quantities (Zhang et al, 2020), and differentiation (Kim et al, 2009;Tiwari et al, 2015). We also found that BPA inhibited neurite outgrowth of PC12 cells and rat primary cultured neuronal cells.…”

Section: Discussionmentioning

confidence: 54%

“…In the present study, we examined the effects of BPF, which is less hydrophobic than BPA, on S-nitrosylation of PDI and neurite outgrowth of PC12 cells. BPA derivatives, such as BPF, are replacing BPA because of its toxicity; however, the effects of BPF on neuronal differentiation are still being debated (Yin et al, 2019;Liang et al, 2020;Fujiwara et al, 2018;Rosenfeld, 2017). BPF and BPA cross the bloodbrain barrier and accumulate in brain tissue (Charisiadis et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

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Bisphenol A and rotenone induce S-nitrosylation of protein disulfide isomerase (PDI) and inhibit neurite outgrowth of primary cultured cells of the rat hippocampus and PC12 cells

et al. 2020

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-Bisphenol A (BPA) interferes the function and development of the central nervous system (CNS), resulting in behavioral abnormalities and memory loss. S-nitrosylation of protein disulfide isomerase (PDI) is increased in brains with sporadic Alzheimer's disease and Parkinson's disease. The aim of the present study was to clarify the role of nitric oxide (NO) in BPA-induced neurotoxicity. Since rotenone induces NO-mediated neurodegeneration through S-nitrosylation of PDI, it was used as a positive control. First, rats were treated with BPA and rotenone, and S-nitrosylation of PDI was detected in rat brain microsomes. BPA and rotenone decreased RNase oxidation activity of PDI concomitant with S-nitrosylation of PDI. Next, to clarify S-nitrosylation of PDI by BPA and rotenone in rat brains, we treated the rat pheochromocytoma cell line PC12 and primary cultured neuron cells from the rat hippocampus with BPA (5 and 10 μM) and rotenone (100 or 200 nM). BPA induced S-nitrosylation of PDI, while NG-monomethyl-L-arginine (L-NMMA), a NOS inhibitor, exerted the opposite effects. Finally, to evaluate the toxicity of BPA in the CNS, we investigated its effects on neurite outgrowth of PC12 and primary cultured neuron cells. BPA inhibited neurite outgrowth of these cells, while L-NMMA reversed this inhibition. The involvement of PDI activity in neurite outgrowth was also examined, and bacitracin, a PDI inhibitor, is shown to decrease neurite outgrowth. Furthermore, the overexpression of PDI, but not a catalytically inactive PDI mutant, enhanced neurite outgrowth. These results suggested that S-nitrosylation of PDI induced by excessive NO caused BPA-induced neurotoxicity.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Bisphenol A and rotenone induce S-nitrosylation of protein disulfide isomerase (PDI) and inhibit neurite outgrowth of primary cultured cells of the rat hippocampus and PC12 cells

et al. 2020

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“…BDE47 has recently been reported to have inhibitory effects on human ES-derived neuronal cells similar to our model [ 21 , 33 ]. Similarly, BPA has been found to have suppressive effects on neuronal stem cells [ 34 , 35 ]. Regarding OH-PCB187 or mother compounds of PCB, epidemiological studies suggest a negative relationship with IQ and a relationship with ADHD [ 36 ], but no report has been made in vitro.…”

Section: Resultsmentioning

confidence: 99%

Early Transcriptomic Changes upon Thalidomide Exposure Influence the Later Neuronal Development in Human Embryonic Stem Cell-Derived Spheres

Kikegawa

Qin

Ito

et al. 2020

IJMS

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Stress in early life has been linked with the development of late-life neurological disorders. Early developmental age is potentially sensitive to several environmental chemicals such as alcohol, drugs, food contaminants, or air pollutants. The recent advances using three-dimensional neural sphere cultures derived from pluripotent stem cells have provided insights into the etiology of neurological diseases and new therapeutic strategies for assessing chemical safety. In this study, we investigated the neurodevelopmental effects of exposure to thalidomide (TMD); 2,2′,4,4′-tetrabromodiphenyl ether; bisphenol A; and 4-hydroxy-2,2′,3,4′,5,5′,6-heptachlorobiphenyl using a human embryonic stem cell (hESC)-derived sphere model. We exposed each chemical to the spheres and conducted a combinational analysis of global gene expression profiling using microarray at the early stage and morphological examination of neural differentiation at the later stage to understand the molecular events underlying the development of hESC-derived spheres. Among the four chemicals, TMD exposure especially influenced the differentiation of spheres into neuronal cells. Transcriptomic analysis and functional annotation identified specific genes that are TMD-induced and associated with ERK and synaptic signaling pathways. Computational network analysis predicted that TMD induced the expression of DNA-binding protein inhibitor ID2, which plays an important role in neuronal development. These findings provide direct evidence that early transcriptomic changes during differentiation of hESCs upon exposure to TMD influence neuronal development in the later stages.

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“…8 It was reported that high BPA concentration is present in canned vegetables and fruits approximately ranging from 3.7 mg/kg to 959 mg/kg, while from 1.0 mg/kg to 223.91 mg/kg was detected in seafood. 8 Numerous health-related issues have been reported due to consumption of BPA and its migration into ecosystem, namely mutagenicity, 9 teratogenicity, 10 obesity, 11 hepatotoxicity, 12 neurotoxicity, 13 and immunotoxicity. 14 Its bioaccumulation has been reported in the trophic level of food chain that can even cause death of fresh water and marine fauna.…”

Section: Introductionmentioning

confidence: 99%

“…17 Animal data revealed that BPA can induce damage in the nervous system by disrupting the function of dopamine system and hippocampus. 13 Mild doses of BPA induces changes in the development of mammary gland and increased frequency of tumors. 18 Hassan et al in 2012 reported the hepatotoxicity due to BPA administration characterized by the formation of reactive oxygen species and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Subchronic toxicity of bisphenol A on the architecture of spleen and hepatic trace metals and protein profile of adult male Wistar rats

et al. 2020

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Bisphenol A (BPA) is one of the widely used chemical as a plasticizer and regarded as endocrine disruptor because of its ability to derail body metabolic functions and adverse effect on the vital organs. The present work outlined the subchronic effect of low-dose BPA (10 mg/kg) on histology of spleen, level of hepatic trace metals, and hepatic protein profile of Wistar rats. To conduct the research work, animals were grouped into two categories ( n = 5). Group 1 was labelled as the control group and group 2 was taken as an experimental group. Experimental group was exposed to low-dose BPA for 12 weeks. Histopathology of spleen highlighted dilation in splenic sinuses, follicle activation, followed by depopulation in the area of white pulp and red pulp in the experimental group. Iron staining revealed significant hemosiderosis in the experimental group when compared with the control group. Statistically significant decrease was noted in zinc and copper concentrations, while nonsignificant change was observed for magnesium concentration through atomic absorption spectroscopy. Sodium dodecyl sulfate–polyacrylamide gel electrophoresis was run for hepatic protein profiling, and as compared to control, elevated levels of different proteins were observed in the experimental group. It can be concluded from the above results that even low dose of BPA causes changes in the major organs of the body. Hence, it is suggested that BPA alternative should be used, so that public health status can be secured.

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Bisphenol A and several derivatives exert neural toxicity in human neuron-like cells by decreasing neurite length

Cited by 42 publications

References 39 publications

Bisphenol A and rotenone induce S-nitrosylation of protein disulfide isomerase (PDI) and inhibit neurite outgrowth of primary cultured cells of the rat hippocampus and PC12 cells

Bisphenol A and rotenone induce S-nitrosylation of protein disulfide isomerase (PDI) and inhibit neurite outgrowth of primary cultured cells of the rat hippocampus and PC12 cells

Early Transcriptomic Changes upon Thalidomide Exposure Influence the Later Neuronal Development in Human Embryonic Stem Cell-Derived Spheres

Subchronic toxicity of bisphenol A on the architecture of spleen and hepatic trace metals and protein profile of adult male Wistar rats

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