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Prenatal 1-Nitropyrene Exposure Causes Autism-Like Behavior Partially by Altering DNA Hydroxymethylation in
Ting Zhao1,2, Cheng-Qing Huang3, Yi-Hao Zhang1,2
1Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, 230022, China.
Summary
Prenatal exposure to motor vehicle exhaust component 1-nitropyrene (1-NP) induces autism-like behaviors in mice by disrupting interneuron migration and altering DNA hydroxymethylation. Maternal alpha-ketoglutarate (α-KG) supplementation mitigates these effects.
Area of Science:
- Neuroscience
- Developmental Biology
- Environmental Health
Background:
- Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by social communication deficits and repetitive behaviors.
- Motor vehicle exhaust contains pollutants like 1-nitropyrene (1-NP), a potential environmental risk factor for neurodevelopmental disorders.
Purpose of the Study:
- To examine the impact of prenatal 1-nitropyrene (1-NP) exposure on the development of autism-like behaviors in a mouse model.
- To elucidate the underlying molecular mechanisms involving interneuron migration and DNA hydroxymethylation.
Main Methods:
- Utilized a mouse model exposed prenatally to 1-NP.
- Conducted behavioral tests (three-chamber test), electrophysiology (patch clamp), immunofluorescence, and molecular analyses of gene expression and DNA modification (TET activity).
- Investigated the therapeutic potential of alpha-ketoglutarate (α-KG) supplementation.
Main Results:
- Prenatal 1-NP exposure led to autism-like behaviors, reduced inhibitory synaptic transmission, and decreased numbers of glutamate decarboxylase 67 (GAD67)-positive interneurons.
- 1-NP exposure impaired interneuron migration by downregulating related genes and inhibiting ten-eleven translocation (TET) activity, reducing DNA hydroxymethylation.
- Maternal α-KG supplementation reversed 1-NP-induced epigenetic changes, interneuron migration deficits, and autism-like behaviors in offspring.
Conclusions:
- Prenatal exposure to 1-nitropyrene is a potential environmental risk factor contributing to autism-like behaviors.
- The mechanism involves impaired interneuron migration due to altered DNA hydroxymethylation of critical genes, mediated by TET enzyme inhibition.
- Maternal α-KG supplementation shows promise in preventing or ameliorating 1-NP-induced neurodevelopmental deficits and autism-like behaviors.
Keywords:
1‐nitropyreneautism‐like behaviorepigenetic reprogramminghydroxymethylationinterneuron migrationMore Related Videos
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