Polychlorinated Diphenylsulfides Activate Aryl Hydrocarbon Receptor 2 in Zebrafish Embryos: Potential Mechanism of Developmental Toxicity

2018 ◽  
Vol 52 (7) ◽  
pp. 4402-4412 ◽  
Author(s):  
Rui Zhang ◽  
Xiaoxiang Wang ◽  
Xuesheng Zhang ◽  
Chao Song ◽  
Robert J. Letcher ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Developmental Toxicity ◽  
Zebrafish Embryos ◽  
Potential Mechanism ◽  
Aryl Hydrocarbon

scholarly journals Cardiovascular Effects of PCB 126 (3,3’,4,4’,5-Pentachlorobiphenyl) in Zebrafish Embryos and Impact of Co-Exposure to Redox Modulating Chemicals

2019 ◽  
Vol 20 (5) ◽  
pp. 1065 ◽  
Author(s):  
Elisabet Teixidó ◽  
Marta Barenys ◽  
Ester Piqué ◽  
Joan Llobet ◽  
Jesús Gómez-Catalán
Keyword(s):  
Oxidative Stress ◽  
Developmental Toxicity ◽  
Environmental Pollutants ◽  
Cardiovascular Effects ◽  
Zebrafish Embryos ◽  
Oxidative Potential ◽  
Antioxidant Genes ◽  
Aryl Hydrocarbon ◽  
Low Concentrations ◽  
Pericardial Edema

The developing cardiovascular system of zebrafish is a sensitive target for many environmental pollutants, including dioxin-like compounds and pesticides. Some polychlorinated biphenyls (PCBs) can compromise the cardiovascular endothelial function by activating oxidative stress-sensitive signaling pathways. Therefore, we exposed zebrafish embryos to PCB126 or to several redox-modulating chemicals to study their ability to modulate the dysmorphogenesis produced by PCB126. PCB126 produced a concentration-dependent induction of pericardial edema and circulatory failure, and a concentration-dependent reduction of cardiac output and body length at 80 hours post fertilization (hpf). Among several modulators tested, the effects of PCB126 could be both positively and negatively modulated by different compounds; co-treatment with α-tocopherol (vitamin E liposoluble) prevented the adverse effects of PCB126 in pericardial edema, whereas co-treatment with sodium nitroprusside (a vasodilator compound) significantly worsened PCB126 effects. Gene expression analysis showed an up-regulation of cyp1a, hsp70, and gstp1, indicative of PCB126 interaction with the aryl hydrocarbon receptor (AhR), while the transcription of antioxidant genes (sod1, sod2; cat and gpx1a) was not affected. Further studies are necessary to understand the role of oxidative stress in the developmental toxicity of low concentrations of PCB126 (25 nM). Our results give insights into the use of zebrafish embryos for exploring mechanisms underlying the oxidative potential of environmental pollutants.

scholarly journals A Truncation in the Aryl Hydrocarbon Receptor of the CRL:WI(Han) Rat Does Not Affect the Developmental Toxicity of TCDD

2008 ◽  
Vol 107 (2) ◽  
pp. 512-521 ◽  
Author(s):  
Tao Jiang ◽  
David R. Bell ◽  
Sally Clode ◽  
Ming Qi Fan ◽  
Alwyn Fernandes ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Developmental Toxicity ◽  
Aryl Hydrocarbon

scholarly journals AHR1B, a new functional aryl hydrocarbon receptor in zebrafish: tandem arrangement of ahr1b and ahr2 genes

2005 ◽  
Vol 392 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Sibel I. Karchner ◽  
Diana G. Franks ◽  
Mark E. Hahn
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Amino Acid Sequence Identity ◽  
Developmental Toxicity ◽  
Physiological Role ◽  
Vertebrate Development ◽  
Chromosome 16 ◽  
Model Species ◽  
High Affinity ◽  
Aryl Hydrocarbon

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates gene expression following activation by TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) or a variety of other synthetic and natural compounds. Previous studies have identified two AHR genes, AHR1 and AHR2, in zebrafish (Danio rerio), a widely used model species for studying vertebrate development and an emerging model in developmental toxicology. Zebrafish AHR2 binds TCDD with high affinity, is transcriptionally active and has a major role in mediating the developmental toxicity of TCDD. Zebrafish AHR1 lacks the ability to bind TCDD and activate transcription, and has no known function. In the present study, we report a new zebrafish AHR, designated AHR1B, which shares 34% amino acid sequence identity with AHR1 (AHR1A). The ahr1b gene resides on chromosome 22, adjacent to ahr2, whereas the ahr1a gene is located on chromosome 16. AHR1B is expressed in embryos as early as 24 hours post-fertilization and increases through the next 2 days, but expression is not inducible by TCDD. In contrast with the previously identified AHR1A, in vitro-expressed AHR1B protein exhibits specific, high-affinity binding of [3H]TCDD. Furthermore, AHR1B is able to activate the transcription of a reporter gene under the control of AHR response elements with an efficacy comparable with that of AHR2, but with a higher EC50. We speculate that AHR1B may have a physiological role, such as in embryonic development, whereas AHR2 mediates the response to xenobiotics.

scholarly journals AhR Antagonist Promotes Differentiation of Papillary Thyroid Cancer via Regulating circSH2B3/miR-4640-5P/IGF2BP2 Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Ri Sa ◽  
Meiliang Guo ◽  
Danyan Liu ◽  
Feng Guan
Keyword(s):  
Thyroid Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Papillary Thyroid Cancer ◽  
Therapeutic Approach ◽  
Potential Mechanism ◽  
Papillary Thyroid ◽  
Aryl Hydrocarbon ◽  
Potential Marker ◽  
First Time ◽  
Novel Therapeutic

Abnormally high expression of aryl hydrocarbon receptor (AhR) has been implicated in dedifferentiation of radioiodine-refractory papillary thyroid cancer (RR-PTC). This study aimed to evaluate the differentiation effect of AhR antagonist in PTC, and to explore the potential mechanism of it. Results showed that AhR antagonists promoted differentiation of PTC, as shown as increase in 125I uptake and Na/I symporter (NIS) expression level. CircRNA microarray in K1 cells treated with StemRegenin 1(SR1) revealed that hsa_circ_0006741 (circSH2B3) was down-regulated in SR1 treated K1 cells. Downregulation of circSH2B3 increased 125I uptake and NIS expression levels. CircSH2B3 acted as an endogenous sponge of hsa-miR-4640-5p and modulated IGF2BP2 expression. IGF2BP2 overexpression induced dedifferentiation of PTC, while silencing IGF2BP2 accelerated differentiation of PTC cells. Rescue studies showed that the dedifferentiation activity of AhR was modulated by the circSH2B3/miR-4640-5p/IGF2BP2 axis. Our findings confirmed for the first time that AhR antagonists promote differentiation of PTC via inhibiting the circSH2B3/miR-4640-5p/IGF2BP2 axis, offering a novel therapeutic approach and a potential marker for differentiation of PTC.

Inhibition of apolipoprotein A-I gene by the aryl hydrocarbon receptor: A potential mechanism for smoking-associated hypoalphalipoproteinemia

Life Sciences ◽  
2012 ◽  
Vol 91 (1-2) ◽  
pp. 64-69 ◽  
Author(s):  
Emad Naem ◽  
Rosalyn Alcalde ◽  
Margaret Gladysz ◽  
Sandra Mesliniene ◽  
Sarada Jaimungal ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Potential Mechanism ◽  
Aryl Hydrocarbon ◽  
Apolipoprotein A ◽  
I Gene
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