Developmental short photoperiod exposure impairs sperm motility in Brandt's voles via antioxidant enzyme-mediated ROS dysregulation.

Photoperiod serves as a critical environmental signal that orchestrates seasonal reproduction in mammals, influencing not only sperm production but also sperm activity. Nevertheless, the molecular basis of this photoperiodic regulation of sperm activity during development remains poorly understood. Here, we show that short photoperiod (8L:16D) exposure during jucenile stage significantly impairs sperm motility in Brandt's voles (Lasiopodomys brandtii), reducing motile sperm percentage, progressive motility, and straight-line velocity, without altering gross sperm morphology. Quantitative proteomics identified 38 differentially expressed proteins between long- and short-photoperiod groups, with Gene Ontology and Gene Set Enrichment Analyses revealing prominent enrichment of reactive oxygen species (ROS)-related pathways. Five core antioxidant proteins-catalase (CAT), peroxiredoxin 1 (PRDX1), peroxiredoxin 2 (PRDX2), thioredoxin 1 (TRX1), and glutaredoxin 2 (GLRX2)-were significantly downregulated in sperm under short photoperiod, as confirmed by western blotting and immunofluorescence. This downregulation led to elevated ROS and superoxide anion levels, reduced mitochondrial membrane potential, increased malondialdehyde content, protein carbonylation, and DNA fragmentation, ultimately culminating in oxidative damage and impaired sperm motility. Our findings demonstrate that photoperiod governs sperm motility in Brandt's voles primarily through modulating antioxidant enzyme expression and ROS homeostasis, providing novel mechanistic insights into seasonal reproductive regulation and identifying potential molecular targets for fertility control and rodent pest management.