Dioxin and Dioxin-Like Compounds Suppress Acetylcholinesterase Activity via Transcriptional Downregulations In Vitro

Xu, Haiming; Xie, Heidi Qunhui; Tao, Wuqun; Zhou, Zhiguang; Li, Shuai-Zhang; Zhao, Bin

doi:10.1007/s12031-013-0167-5

Cited by 17 publications

(24 citation statements)

References 28 publications

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“…Nevertheless, other TnBP concentrations significantly suppressed AChE activity of PC12 cells in Figure 3B. This was similar to the findings of Xu et al who found out that AChE activity and expression level can be down regulated by 2,3,7,8‐tetrachloro dibenzo‐para‐dioxin (TCDD) in neuronal cells 36 …”

Section: Resultssupporting

confidence: 90%

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Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

Chang

Cui

Jiang

et al. 2020

Environmental Toxicology

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Organophosphate flame retardants (OPFRs) have become a growing concern due to their potential environmental and health risk. However, limited studies have described the toxicity, particularly neurotoxicity of alkyl and aromatic OPFRs. This study investigated the neurotoxicity of alkyl tri‐n‐butyl phosphate (TnBP) and aromatic tricresyl phosphate (TCP) to rat adrenal pheochromocytoma (PC12) cells for 24 h. Viability detection showed dose‐response toxicity effect of TCP and TnBP to PC12 cells. The half‐maximal inhibitory concentration of 24 h (24 h‐IC50) of TCP and TnBP were 2415.61 and 338.09 μM, respectively. Both TnBP and TCP significantly changed the acetylcholinesterase (AChE) activity, and TnBP is more likely to cause neurotoxicity to PC12 cells compared to TCP. Also, The results of LDH and caspase‐3 activity detection as well as Hoechst staining suggested that cell apoptosis induced by TCP and TnBP may be the primary pathway. These findings provide a toxicity data of aromatic and alkyl‐substituted OPFRs to PC12 cells, and a new insight into the toxicity of OPFRs on health risk assessment.

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Section: Resultssupporting

confidence: 90%

“…This was similar to the findings of Xu et al who found out that AChE activity and expression level can be down regulated by 2,3,7,8-tetrachloro dibenzo-para-dioxin (TCDD) in neuronal cells. 36 PC12 is a well-studied cell model for neuronal differentiation.…”

Section: Cell Morphologymentioning

confidence: 99%

Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

Chang

Cui

Jiang

et al. 2020

Environmental Toxicology

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“…A human neuroblastoma cell line, SK-N-SH cell, exhibits numerous biochemical characteristics of neurons, and has been employed as a model of human neurons to investigate the toxicity of dioxins 6 , 24 . In the current study, we adopted miR microarray analyses to perform global analysis of differentially expressed miRs caused by dioxins.…”

Section: Introductionmentioning

confidence: 99%

CDC42 expression is altered by dioxin exposure and mediated by multilevel regulations via AhR in human neuroblastoma cells

Xie

et al. 2017

Sci Rep

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Emerging evidence has shown that dioxin causes dysregulation of microRNAs (miRs) in a variety of tissues or cells. However, little is known about dioxin effects on neuronal miRs expression. In the present study, 277 differentially expressed miRs were identified by miRs microarray analysis in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, at 10−10 M) treated SK-N-SH neuroblastoma cells. Among them, 53 miRs exhibited changes of more than 0.4-fold. Consistent with the microarray data, we verified the induction effect of TCDD on hsa-miR-608 expression, which is a primate-specific miR associated with brain functions. Bioinformatics analysis showed involvement of hsa-miR-608 in cytoskeleton organization, in which one of the hsa-miR-608 target genes, Cell Division Cycle 42 (CDC42), might play a role. We also confirmed induction of CDC42 expression by TCDD in SK-N-SH cells. TCDD induced the expression of CDC42 mRNA in hsa-miR-608 inhibitor transfected cells more obviously than in control cells, suggesting involvement of both transcriptional and post-transcriptional mechanisms in the TCDD-induced CDC42 regulation. Furthermore, CH223191, an antagonist of the aryl hydrocarbon receptor (AhR), counteracted TCDD-induced hsa-miR-608 and CDC42 expression. These results indicated that AhR not only mediates transcriptional induction of CDC42, but also hsa-miR-608-induced post-transcriptional regulation of CDC42 in dioxin treated neuroblastoma cells.

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“…Similarly, other AhR ligands such as 1,2,3,7,8-pentachlorodibenzo- p -dioxin (1,2,3,7,8-PCDD), 2,3,7,8-tetrachlorodibenzofuran (2,3,7,8-TCDF), 2,3,4,7,8-pentachlorodi-benzofuran (2,3,4,7,8-PCDF), and 2,3,7,8-tetrabromodibenzo- p -dioxin (2,3,7,8-TBDD) also suppressed neuronal AChE activity via AhR-mediated transcriptional downregulation. 96 These studies provided important new insights into the mechanisms underlying a neurotransmission impairment characteristic of a number of neurodegenerative diseases. Thus, AhR emerges as an important chemoreceptor in sensing and responding to chemical signals in the nervous system.…”

Section: Ahr-mediated Health Effectsmentioning

confidence: 99%

The Aryl Hydrocarbon Receptor: A Key Bridging Molecule of External and Internal Chemical Signals

Tian

et al. 2015

Environ. Sci. Technol.

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The aryl hydrocarbon receptor (AhR) is a highly evolutionary conserved, ligand-activated transcription factor that is best known to mediate the toxicities of dioxins and dioxin-like compounds. Phenotype of AhR-null mice, together with the recent discovery of a variety of endogenous and plant-derived ligands, point to the integral roles of AhR in normal cell physiology, in addition to its roles in sensing the environmental chemicals. Here, we summarize the current knowledge about AhR signaling pathways, its ligands and AhR-mediated effects on cell specialization, host defense and detoxification. AhR-mediated health effects particularly in liver, immune, and nervous systems, as well as in tumorgenesis are discussed. Dioxin-initiated embryotoxicity and immunosuppressive effects in fish and birds are reviewed. Recent data demonstrate that AhR is a convergence point of multiple signaling pathways that inform the cell of its external and internal environments. As such, AhR pathway is a promising potential target for therapeutics targeting nervous, liver, and autoimmune diseases through AhR ligand-mediated interventions and other perturbations of AhR signaling. Additionally, using available laboratory data obtained on animal models, AhR-centered adverse outcome pathway analysis is useful in reexamining known and potential adverse outcomes of specific or mixed compounds on wildlife.

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Dioxin and Dioxin-Like Compounds Suppress Acetylcholinesterase Activity via Transcriptional Downregulations In Vitro

Abstract: Recently, acetylcholinesterase (AChE, EC 3.1

Cited by 17 publications

References 28 publications

Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

CDC42 expression is altered by dioxin exposure and mediated by multilevel regulations via AhR in human neuroblastoma cells

The Aryl Hydrocarbon Receptor: A Key Bridging Molecule of External and Internal Chemical Signals

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