Acrylamide-induced oxidative stress triggers organelle dysfunction, DNA damage, and apoptosis in porcine embryo development.

Acrylamide (ACR) forms in carbohydrate-rich foods during cooking at high temperatures and is a common contaminant in the diet. Although ACR has neurotoxic, genotoxic, and carcinogenic effects, limited information is available regarding its reproductive toxicity. This study was performed to investigate the effects of ACR exposure on porcine embryonic development and to elucidate the underlying mechanisms. Following parthenogenetic activation and in vitro fertilization, ACR exposure significantly reduced developmental parameters, including the cleavage rate, proportion of 4-cell stage embryos, and blastocyst formation rate, compared with controls. ACR exposure delayed development during the post-blastulation period and decreased cell numbers and survival. In addition, ACR exposure impaired RNA transcription, DNA replication, protein synthesis, and zygotic genome activation. ACR disrupted the Nrf2/Keap1 signaling pathway and resulted in elevated levels of reactive oxygen species and decreased glutathione levels compared to controls. It also significantly increased DNA damage and early apoptosis, and altered the transcript levels of genes associated with DNA damage and apoptosis. Moreover, ACR exposure impaired the functions of the mitochondria and endoplasmic reticulum. In conclusion, ACR exposure had detrimental effects on porcine embryonic development by inducing oxidative stress that led to DNA damage, apoptosis, and organelle dysfunction.