Pyrroloquinoline quinone protects heat-stressed porcine oocytes and improves early embryonic development via maintaining mitochondrial integrity and redox homeostasis.

Heat stress (HS) is a major environmental factor that impairs female fertility by disrupting oocyte quality and developmental competence. Pyrroloquinoline quinone (PQQ), a redox cofactor with strong antioxidant and mitochondrial-protective properties, has recently attracted attention for its cytoprotective roles in mammalian cells. Here, we investigated whether PQQ supplementation could alleviate HS-induced porcine oocyte damage and improve subsequent embryonic development. Our results showed that PQQ treatment significantly restored the rates of germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE) in heat-stressed oocytes. PQQ markedly reduced intracellular reactive oxygen species (ROS) accumulation, enhanced mitochondrial membrane potential (ΔΨm), and maintained ATP levels, indicating improved mitochondrial function. Furthermore, PQQ attenuated DNA damage (γH2A.X foci) and apoptosis (Caspase-3 activation), preserved spindle morphology and actin distribution, and normalized cortical granule and ovastacin localization, suggesting improved cytoplasmic maturation. Importantly, embryos derived from PQQ-treated oocytes exhibited higher cleavage and blastocyst formation rates compared with the HS group. Collectively, these findings demonstrate that PQQ effectively mitigates HS-induced oocyte dysfunction by maintaining mitochondrial integrity, redox balance, and cytoskeletal organization, thereby improving oocyte competence and early embryonic development under heat stress.