Spermidine counters homosalate reproductive toxicity in mouse oocytes by preserving mitochondria and cytoskeleton

Mouse oocytes treated with homosalate showed delayed meiotic progression, oxidative stress, DNA damage, early apoptosis, and reduced mitochondrial function. Spermidine supplementation preserved mitochondrial membrane potential, ATP production, and oxidative phosphorylation gene expression. It also stabilized spindle structure, F-actin assembly, and kinetochore-microtubule attachments, which lowered aneuploidy risk. The findings suggest spermidine can blunt certain environmental toxicant effects on oocyte quality.