Triphenyl phosphate interferes with the synthesis of steroid hormones through the PPARγ/CD36 pathway in human trophoblast JEG‐3 cells DOI
Yuting Chen, Qian Liu, Yao Wang

et al.

Environmental Toxicology, Journal Year: 2024, Volume and Issue: 39(6), P. 3400 - 3409

Published: March 7, 2024

Abstract Triphenyl phosphate (TPhP), a chemical commonly found in human placenta and breast milk, has been shown to disturb the endocrine system. Our previous study confirmed that TPhP could accumulate interference with placental lipid metabolism steroid hormone synthesis, as well induce endoplasmic reticulum (ER) stress through PPARγ trophoblast JEG‐3 cells. However, molecular mechanism underlying this disruption remains unknown. aimed identify role of PPARγ/CD36 pathway TPhP‐induced disruption. We increased accumulation, total cholesterol, low‐ high‐density protein progesterone, estradiol, glucocorticoid, aldosterone levels, genes related hormones including 3βHSD1 , 17βHSD1 CYP11A CYP19 CYP21 . These effects were largely blocked by co‐exposure either antagonist GW9662 or knockdown CD36 using siRNA (siCD36). Furthermore, an ER inhibitor 4‐PBA attenuated effect on progesterone glucocorticoid siCD36 reduced stress‐related levels induced TPhP, BiP, PERK, CHOP. findings suggest may also play synthesis TPhP. As our shed light pathway's involvement disturbance biosynthesis cells, further investigations potential impacts function following birth outcome are warranted.

Language: Английский

Triphenyl phosphate disrupts placental tryptophan metabolism by activating MAOA/ROS/NFκB DOI

Xiaoxun Lu,

Jiabin Hong,

Jing Zhang

et al.

The Science of The Total Environment, Journal Year: 2023, Volume and Issue: 904, P. 166688 - 166688

Published: Sept. 1, 2023

Language: Английский

Citations

7
Roxithromycin exposure induces motoneuron malformation and behavioral deficits of zebrafish by interfering with the differentiation of motor neuron progenitor cells DOI Creative Commons
Wenjie Xie, Juntao Chen, Xiaoqian Cao

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 276, P. 116327 - 116327

Published: April 15, 2024

Roxithromycin (ROX), a commonly used macrolide antibiotic, is extensively employed in human medicine and livestock industries. Due to its structural stability resistance biological degradation, ROX persists as resilient environmental contaminant, detectable aquatic ecosystems food products. However, our understanding of the potential health risks humans from continuous exposure remains limited. In this study, we zebrafish vertebrate model explore developmental toxicity early exposure, particularly focusing on effects locomotor functionality CaP motoneuron development. Early induces marked embryos, significantly reducing hatching rates (n=100), body lengths increased malformation (n=100). The embryos treated with corresponding volume DMSO (0.1%, v/v) served vehicle controls (veh). Moreover, adversely affected locomotive capacity observations transgenic Tg(hb9:eGFP) revealed axonal loss motor neurons, evident through reduced or irregular (n=80). Concurrently, abnormal apoptosis ROX-exposed intensified alongside upregulation apoptosis-related genes (bax, bcl2, caspase-3a). Single-cell sequencing further disclosed substantial involved differentiation neuron progenitor cells (ngn1, olig2), axon development (cd82a, mbpa, plp1b, sema5a), neuroimmunity (aplnrb, aplnra) larvae (n=30). Furthermore, defects behavioral deficits induced by can be rescued administering ngn1 agonist summary, leads early-life abnormalities neurons behavior hindering inducing apoptosis.

Language: Английский

Citations

2
Physiological and transcriptomic changes of zebrafish (Danio rerio) in response to Isopropylate Triphenyl Phosphate (IPPP) exposure DOI
Qiong Zhang,

Shukai Zheng,

Xiaoling Shi

et al.

Environmental Toxicology and Pharmacology, Journal Year: 2024, Volume and Issue: 110, P. 104528 - 104528

Published: Aug. 8, 2024

Language: Английский

Citations

2
Apoptotic mechanism of development inhibition in zebrafish induced by esketamine DOI Creative Commons
Wenjuan Yuan, Yinggang Xiao, Yang Zhang

et al.

Toxicology and Applied Pharmacology, Journal Year: 2023, Volume and Issue: 482, P. 116789 - 116789

Published: Dec. 15, 2023

Esketamine, a widely used intravenous general anesthetic, is also employed for obstetric and pediatric anesthesia, depression treatment. However, concerns regarding esketamine abuse have emerged. Moreover, the potential in vivo toxicity of on growth development remains unclear. To address these concerns, we investigated effects exposure developmental parameters, cell apoptosis, gene expression zebrafish. Esketamine concentration-dependently decreased heart rate body length zebrafish embryos/larvae while increasing hatching spontaneous movement frequency. Developmental retardation larvae, including shallow pigmentation, small eyes, delayed yolk sac absorption, was observed following altered apoptosis-related genes heads, primarily downregulating bax, caspase9, caspase3, caspase6, caspase7. Intriguingly, BTSA1, Bax agonist, reversed anti-apoptotic decelerated Collectively, our findings suggest that may hinder embryonic by inhibiting apoptosis via Bax/Caspase9/Caspase3 pathway. best knowledge, this first study to report lethal We elucidated toxic larvae its apoptotic mechanisms. Further studies are warranted evaluate safety animals humans.

Language: Английский

Citations

6
Triphenyl phosphate interferes with the synthesis of steroid hormones through the PPARγ/CD36 pathway in human trophoblast JEG‐3 cells DOI
Yuting Chen, Qian Liu, Yao Wang

et al.

Environmental Toxicology, Journal Year: 2024, Volume and Issue: 39(6), P. 3400 - 3409

Published: March 7, 2024

Abstract Triphenyl phosphate (TPhP), a chemical commonly found in human placenta and breast milk, has been shown to disturb the endocrine system. Our previous study confirmed that TPhP could accumulate interference with placental lipid metabolism steroid hormone synthesis, as well induce endoplasmic reticulum (ER) stress through PPARγ trophoblast JEG‐3 cells. However, molecular mechanism underlying this disruption remains unknown. aimed identify role of PPARγ/CD36 pathway TPhP‐induced disruption. We increased accumulation, total cholesterol, low‐ high‐density protein progesterone, estradiol, glucocorticoid, aldosterone levels, genes related hormones including 3βHSD1 , 17βHSD1 CYP11A CYP19 CYP21 . These effects were largely blocked by co‐exposure either antagonist GW9662 or knockdown CD36 using siRNA (siCD36). Furthermore, an ER inhibitor 4‐PBA attenuated effect on progesterone glucocorticoid siCD36 reduced stress‐related levels induced TPhP, BiP, PERK, CHOP. findings suggest may also play synthesis TPhP. As our shed light pathway's involvement disturbance biosynthesis cells, further investigations potential impacts function following birth outcome are warranted.

Language: Английский

Citations

2