Spermidine supplementation protects porcine oocytes from triclosan-induced meiotic and fertilization defects by attenuating oxidative stress-mediated apoptosis

Abstract Oocytes are highly susceptible to environmental pollutants, with triclosan (TCS)—a pervasive antimicrobial—known to bioaccumulate and impair reproductive function. However, mechanisms driving TCS-induced oocyte degeneration and effective protective approaches remain unclear. This study investigates the protective effects of spermidine against TCS-induced meiotic disruption and fertilization defects in porcine oocytes, exploring its antioxidant and anti-apoptotic mechanisms. Porcine germinal vesicle (GV) oocytes were exposed in vitro to graded TCS concentrations (0.5–5 μM) with or without spermidine supplementation. Meiotic maturation, reactive oxygen species (ROS) production, DNA damage, mitochondrial function, apoptosis, and fertilization competence were assessed using immunofluorescence, fluorescence quantification, and mitochondrial distribution analyses. TCS exposure disrupted meiotic progression, causing spindle defects, chromosome misalignment, mitochondrial dysfunction, elevated ROS, DNA damage, and apoptosis, reducing maturation and fertilization rates. Spermidine significantly reversed these effects by stabilizing cytoskeletal architecture, lowering oxidative stress, and inhibiting apoptosis, thereby improving oocyte quality and developmental competence. Spermidine effectively attenuates TCS-induced meiotic and fertilization impairments by mitigating oxidative stress-mediated apoptosis, offering promising intervention strategies to preserve oocyte quality under environmental toxicant exposure.