Single-cell transcriptomics unveils PM2.5 exposure-induced mouse reproductive damage linked to embryonic developmental defects.

This study employed C57BL/6 male mice to examine the effects of PM2.5 exposure on male reproductive function and early embryonic development. Single-cell transcriptomic analysis revealed significant DNA damage and metabolic dysregulation in the testicular tissues of PM2.5-exposed mice, starting at the undifferentiated spermatogonia stage. Untargeted metabolomics further identified metabolic disturbances in sperm, with notable alterations in key pathways, including galactose metabolism, glycine, serine, and threonine metabolism, and nucleotide metabolism. PM2.5 exposure significantly impaired sperm motility, thereby reducing its fertilizing capacity. Although the blastocyst formation rate in the PM2.5-exposed group did not differ significantly from that of the Control group, clear developmental delays were observed in peri-implantation embryos, accompanied by substantial transcriptomic abnormalities. Notably, pronounced dysregulation in differentially expressed genes was already evident at the 2-cell and blastocyst stages, suggesting that PM2.5 exposure may disrupt subsequent developmental processes by altering gene expression patterns in pre-implantation embryos.