Centre de Recherche en Reproduction, Développement et Santé Intergénérationnelle, Université Laval, Québec, Québec G1V 0A6, Canada;
To whom correspondence should be addressed at Chaire de Recherche du Canada en Génomique Animale, Université Laval, Département des Sciences Animales, Pavillon des Services, INAF, bureau 2732 Université Laval, Québec, Québec G1V 0A6, Canada. E-mail: email@example.com
Alcohol consumption during pregnancy is still a cause of preventable birth defects and developmental disabilities. However, little is known about the impact of ethanol on preimplantation embryos and the molecular mechanisms involved. We aimed to determine the toxicogenomic impacts and the mechanisms involved in preimplantation embryonic survival following 0.2% ethanol exposure in porcine embryos. Gene expression changes were measured with a porcine embryo specific microarray and confirmed by RT-qPCR. When compared with control, ethanol exposure led to a 43% decrease in blastocyst rate and activated pathways associated with oxidative stress and nervous system damage, such as TP53 and TGF. Moreover, we observed a mitochondrial dysfunction in the exposed embryos as revealed by the decrease in Mitotracker Red fluorescence intensity (25 and 41% in 4-cell embryos and blastocysts, respectively) and a modification in the expression of GABRB3, APP, CLU, and MIOX genes. We therefore present evidence of neuronal-like adverse effects on undifferentiated cells suggesting that fetal alcohol spectrum disorder could have its origin as early as in the first week postfertilization.