PCB126 exposure during pregnancy alters maternal and fetal gene expression

• Published in: Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2023-08, Vol.119, p.108385-108385, Article 108385
• Main Authors: Rashid, Cetewayo S., Preston, Joshua D., Ngo Tenlep, Sara Y., Cook, Marissa K., Blalock, Eric M., Zhou, Changcheng, Swanson, Hollie I., Pearson, Kevin J.
• Format: Article
• Language: English
• Subjects: Animals; Aryl Hydrocarbon Receptor; Cytochrome P450; Developmental Toxicity; Endocrine-Disrupting Chemicals; Epigenesis, Genetic; Female; Fetus - metabolism; Gene Expression; Humans; Mice; Polychlorinated Biphenyls - metabolism; Polychlorinated Biphenyls - toxicity; Polychlorinated Biphenyls, Persistent Organic Pollutants; Pregnancy; Receptors, Aryl Hydrocarbon - genetics; Receptors, Aryl Hydrocarbon - metabolism
• ISSN: 0890-6238; 1873-1708; 1873-1708
• DOI: 10.1016/j.reprotox.2023.108385

Polychlorinated biphenyls (PCBs) are organic pollutants that can have lasting impacts on offspring health. Here, we sought to examine maternal and fetal gene expression differences of aryl hydrocarbon receptor (AHR)-regulated genes in a mouse model of prenatal PCB126 exposure. Female mice were bred and gavaged with 1 µmole/kg bodyweight PCB126 or vehicle control on embryonic days 0 and 14, and maternal and fetal tissues were collected on embryonic day 18.5. Total RNAs were isolated, and gene expression levels were analyzed in both maternal and fetal tissues using the NanoString nCounter system. Interestingly, we found that the expression levels of cytochrome P450 (Cyp)1a1 and Cyp1b1 were significantly increased in response to PCB exposure in the tested maternal and fetal tissues. Furthermore, PCB exposure altered the expression of several other genes related to energy balance, oxidative stress, and epigenetic regulation in a manner that was less consistent across tissue types. These results indicate that maternal PCB126 exposure significantly alters gene expression in both developing fetuses and pregnant dams, and such changes vary in intensity and expressivity depending on tissue type. The altered gene expression may provide insights into pathophysiological mechanisms by which in utero PCB exposures contribute to PCB-induced postnatal metabolic diseases. [Display omitted] •Gestational exposure of mice to a dioxin-like PCB did not affect fecundity.•PCB126 exposure upregulated xenobiotic metabolism genes in dams and fetuses.•Genes related to energy balance were altered in a tissue-specific manner.•Gene expression changes in fetal tissues could affect long-term health in offspring.