Thermotolerance and antiapoptosis enhancement by Lycium barbarum polysaccharide: counteracting mitochondrial oxidative stress in human sperm exposed to decabromodiphenyl ether (BDE-209) at 37 °C

Sperm damage resulting from exposure to environmental toxicants or elevated temperatures frequently involves overlapping mechanisms, most notably the induction of mitochondrial oxidative stress. Lycium barbarum polysaccharide (LBP), a bioactive dietary component, mitigates decabromodiphenyl ether (BDE-209)-induced human sperm toxicity by modulating oxidative stress and apoptosis. Exposure to environmentally relevant levels of BDE-209 (40-80 μmol/L) significantly impaired sperm quality, as evidenced by reduced motility, compromised membrane and acrosome integrity, and increased DNA fragmentation when compared to the control group at 37 °C. Mechanistically, exposure to BDE-209 induces mitochondrial oxidative stress, resulting in reactive oxygen species (ROS) accumulation, decreased mitochondrial membrane potential (MMP), and reduced ATP production. This is evidenced by increased activities of Caspase3 and Caspase9, elevated levels of BAX, and decreased expression of BCL-2. LBP intervention (100 μg/mL) effectively scavenged ROS, restored mitochondrial potential, and enhanced antioxidant capacity, as demonstrated by increased superoxide dismutase (SOD) and glutathione (GSH) levels, alongside decreased malondialdehyde (MDA) levels. Furthermore, LBP suppressed apoptotic pathways and enhanced sperm-zona pellucida binding after BDE-209 exposure. A proposed mechanism summarizing this protective pathway is presented in the Graphical . As a naturally occurring polysaccharide that protects against oxidative stress in sperm, LBP could represent a promising candidate for dietary interventions in populations exposed to elevated levels of BDE-209. This warrants further investigation in in vivo models.