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27. Evaluating the Effect of Gestational Exposure to Perfluorohexane Sulfonate on Placental Development in Mice Combining Alternative Splicing and Gene Expression Analyses

Author

Zhang, Yihao, Lv, Jia, Fan, Yi-Jun, Tao, Lin, Xu, Jingjing, Tang, Weitian, Sun, Nan, Zhao, Ling-Li, Xu, De- Xiang, and Huang, Yichao

Subjects
Amides -- Analysis, Genes -- Analysis, Mass spectrometry -- Analysis, Liquid chromatography -- Analysis, RNA -- Analysis, Pregnant women -- Analysis, Euthanasia -- Analysis, Gene expression -- Analysis, Fluorine compounds -- Analysis, Metabolites -- Analysis, Amino acids -- Analysis, Genetic engineering -- Analysis, Epidemiology -- Analysis, Environmental issues, Health, European Union
Abstract

Background: Perfluorohexane sulfonate (PFHxS) is a frequently detected per- and polyfluoroalkyl substance in most populations, including in individuals who are pregnant, a period critical for early life development. Despite epidemiological evidence of exposure, developmental toxicity, particularly at realistic human exposures, remains understudied. Objectives: We evaluated the effect of gestational exposure to human-relevant body burden of PFHxS on fetal and placental development and explored mechanisms of action combining alternative splicing (AS) and gene expression (GE) analyses. Methods: Pregnant ICR mice were exposed to 0, 0.03, and 0.3 [micro]g/kg/day from gestational day 7 to day 17 via oral gavage. Upon euthanasia, PFHxS distribution was measured using liquid chromatography-tandem mass spectrometry. Maternal and fetal phenotypes were recorded, and histopathology was examined for placenta impairment. Multiomics was adopted by combining AS and GE analyses to unveil disruptions in mRNA quality and quantity. The key metabolite transporters were validated by quantitative real-time PCR (qRT-PCR) for quantification and three-dimensional (3D) structural simulation by AlphaFold2. Targeted metabolomics based on liquid chromatography-tandem mass spectrometry was used to detect amino acid and amides levels in the placenta. Results: Pups developmentally exposed to PFHxS exhibited signs of intrauterine growth restriction (IUGR), characterized by smaller fetal weight and body length (p Discussion: The findings from this study suggest that exposure to human-relevant very-low-dose PFHxS during pregnancy in mice caused IUGR, likely via downregulating of placental amino acid transporters, thereby impairing placental amino acid transportation, resulting in impairment of placental development. Our findings confirm epidemiological findings and call for future attention on the health risk of this persistent yet ubiquitous chemical in the early developmental stage and provide a new approach for understanding gene expression from both quantitative and qualitative omics approaches in toxicological studies. https://doi.org/10.1289/EHP13217, Introduction Per- and polyfluoroalkyl substances (PFAS) are a large group of fluorine-containing chemicals commonly applied in industrial and commercial products, resulting in ubiquitous presence in the environment (1,2) and attracting [...]

Published
2023
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46. Prenatal 1‐Nitropyrene Exposure Causes Autism‐Like Behavior Partially by Altering DNA Hydroxymethylation in Developing Brain.

Author

Zhao, Ting, Huang, Cheng‐Qing, Zhang, Yi‐Hao, Zhu, Yan‐Yan, Chen, Xiao‐Xi, Wang, Tao, Shao, Jing, Meng, Xiu‐Hong, Huang, Yichao, Wang, Hua, Wang, Hui‐Li, Wang, Bo, and Xu, De‐Xiang

Subjects
PRENATAL exposure, ANIMAL weaning, GLUTAMATE decarboxylase, AUTISM spectrum disorders, NEURAL transmission
Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder, characterized by social communication disability and stereotypic behavior. This study aims to investigate the impact of prenatal exposure to 1‐nitropyrene (1‐NP), a key component of motor vehicle exhaust, on autism‐like behaviors in a mouse model. Three‐chamber test finds that prenatal 1‐NP exposure causes autism‐like behaviors during the weaning period. Patch clamp shows that inhibitory synaptic transmission is reduced in medial prefrontal cortex of 1‐NP‐exposed weaning pups. Immunofluorescence finds that prenatal 1‐NP exposure reduces the number of prefrontal glutamate decarboxylase 67 (GAD67) positive interneurons in fetuses and weaning pups. Moreover, prenatal 1‐NP exposure retards tangential migration of GAD67‐positive interneurons and downregulates interneuron migration‐related genes, such as Nrg1, Erbb4, and Sema3F, in fetal forebrain. Mechanistically, prenatal 1‐NP exposure reduces hydroxymethylation of interneuron migration‐related genes through inhibiting ten‐eleven translocation (TET) activity in fetal forebrain. Supplement with alpha‐ketoglutarate (α‐KG), a cofactor of TET enzyme, reverses 1‐NP‐induced hypohydroxymethylation at specific sites of interneuron migration‐related genes. Moreover, α‐KG supplement alleviates 1‐NP‐induced migration retardation of interneurons in fetal forebrain. Finally, maternal α‐KG supplement improves 1‐NP‐induced autism‐like behaviors in weaning offspring. In conclusion, prenatal 1‐NP exposure causes autism‐like behavior partially by altering DNA hydroxymethylation of interneuron migration‐related genes in developing brain. [ABSTRACT FROM AUTHOR]

Published
2024
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