Fumonisin B1 (FB1), a mycotoxin commonly found in contaminated food and feed, has been increasingly implicated in neurotoxicity, although its mechanisms remain poorly understood. This study investigates the neurotoxic potential of FB1 in human SH-SY5Y neuroblastoma cells, both undifferentiated and RA-differentiated, and evaluates the protective effect of bromelain, a natural proteolytic enzyme with antioxidant and anti-inflammatory properties. Cells were exposed to 50 μM FB1 for 24 h, with or without co-treatment with bromelain (10 or 50 μg/mL). FB1 significantly reduced cell viability and triggered reactive oxygen species (ROS) production, mitochondrial membrane depolarization, lipid peroxidation, inflammatory cytokine release (IL-6 and TNF-α), and apoptosis, particularly in differentiated cells. Bromelain co-treatment attenuated these effects in a dose-dependent manner, preserving mitochondrial function, reducing oxidative and inflammatory markers, and lowering apoptotic cell death. These findings emphasize the neurotoxic risk posed by FB1 and highlight bromelain as a promising multi-target protective agent. Identifying effective countermeasures against environmental neurotoxins is crucial for public health and disease prevention.
Franco et al. (Tue,) studied this question.