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Sex-specific impacts of prenatal bisphenol A exposure on genes associated with cortical development, social behaviors, and autism in the offspring’s prefrontal cortex
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Researchers found that prenatal exposure to bisphenol A (BPA) — a chemical found in some plastics and food can linings — disrupted the expression of genes in the prefrontal cortex linked to brain development, social behavior, and autism spectrum disorder, with the effects differing significantly between male and female offspring. The findings suggest BPA exposure during pregnancy may contribute to sex differences observed in autism-related brain changes.
This is the first study to show that prenatal BPA exposure dysregulated the expression of ASD-related genes and functions, including cortical neuritogenesis and development and social behaviors, in a sex-dependent manner. Our findings suggest that, besides the hippocampus, BPA could also exert its adverse effects through sex-specific molecular mechanisms in the offspring's prefrontal cortex, which in turn would lead to sex differences in ASD-related neuropathology and clinical manifestations, which deserves further investigation.
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Sex-specific effects of prenatal bisphenol A exposure on transcriptome-interactome profiles of autism candidate genes in neural stem cells from offspring hippocampus
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Researchers exposed pregnant rats to bisphenol A (BPA), a chemical found in many plastics, and examined how it affected the brain stem cells of offspring, finding that male pups showed significantly greater disruption to genes linked to autism spectrum disorder. The results suggest that prenatal BPA exposure may contribute to the higher rates of autism seen in males by altering how key brain genes are expressed during early development.
Sex differences in the effects of prenatal bisphenol A exposure on autism-related genes and their relationships with the hippocampus functions
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Researchers examined how prenatal bisphenol A exposure affects autism-related genes and hippocampal function in rat offspring. The study found that BPA exposure disrupted neurite growth and gene expression in both sexes, but reduced neuronal viability and impaired learning and memory only in male offspring, suggesting sex-dependent vulnerability that may relate to the higher prevalence of autism spectrum disorder in males.
Autism-Related Transcription Factors Underlying the Sex-Specific Effects of Prenatal Bisphenol A Exposure on Transcriptome-Interactome Profiles in the Offspring Prefrontal Cortex
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Researchers found that prenatal bisphenol A exposure disrupted transcriptome-interactome profiles in the prefrontal cortex of neonatal rats in a sex-specific manner, with BPA-responsive genes significantly overlapping with known autism spectrum disorder candidate genes.
Prenatal bisphenol A exposure perturbs sex-dependent transcriptomic regionalization of autism-associated genes in the developing brain
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Researchers reanalyzed published RNA-sequencing data from rat offspring prenatally exposed to BPA and found that BPA disrupted transcriptomic regionalization between the hippocampus and prefrontal cortex in a sex-dependent manner, altering the regional expression of autism-associated genes including Msx2 and Syncrip, with changes correlating with behavioral outcomes.
Investigation of autism-related transcription factors underlying sex differences in the effects of bisphenol A on transcriptome profiles and synaptogenesis in the offspring hippocampus
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Researchers investigated how prenatal bisphenol A (BPA) exposure affects autism-related gene expression differently in male and female rat offspring. The study found sex-specific differences in transcription factor activity and synaptogenesis in the hippocampus, with the androgen receptor playing a key role in BPA-mediated regulation of autism candidate genes.
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