Multi-omics analysis reveals the molecular mechanism of silibinin rescue the toxic effects of butyl benzyl phthalate on porcine preimplantation embryos.

Butyl benzyl phthalate (BBP), a widely used plasticizer and solvent, has raised concerns due to its pervasive presence in the environment and human bodies, prompting worries about its potential health risks. This study aims to uncover the impact of BBP on pre-implantation embryo development and its underlying mechanisms. The experimental results indicate that BBP exposure significantly inhibits the development process of early embryos, reducing the proportion of embryos reaching key formation stages. Through transcriptomic and metabolomic analyses, we found that BBP exposure leads to marked changes in gene expression and metabolite levels associated with mitochondrial function and protein translation, accompanied by structural damage to the endoplasmic reticulum and Golgi apparatus. The study also reveals that BBP may disrupt mitochondrial function through interaction with the mitochondrial membrane protein NDUFA11, thereby inducing oxidative stress and apoptosis. The innovation of this research lies in proposing that silibinin, a natural antioxidant, can effectively alleviate BBP-induced developmental disorders in embryos, offering a new strategy for protecting maternal reproductive health. This work not only provides a scientific basis for understanding the embryotoxicity of BBP but also offers important insights for the health risk assessment and prevention of environmental endocrine disruptors.