Naringenin protects zebrafish larvae from BMAA-induced neuromuscular toxicity by regulating myogenic and inflammatory pathways

β-N-methylamino- L -alanine (BMAA) is an environmental neurotoxin widely detected in aquatic ecosystems and linked to neurodegenerative diseases. While its central neurotoxicity is well documented, its direct effects on skeletal muscle and neuromuscular junctions (NMJs) remain unclear. Naringenin (NAR), a citrus flavanone with antioxidant and anti-inflammatory properties, has shown protective effects in several disease models but has not been evaluated against BMAA-induced toxicity. Here, we used zebrafish larvae to examine the developmental, functional, structural, and molecular effects of BMAA exposure and to assess the protective potential of NAR. Exposure to BMAA caused developmental abnormalities, locomotor impairments, muscle fiber disorganization, and NMJ disruption, accompanied by downregulation of myogenic regulators ( myf5 , myog , myhz2 ) and upregulation of inflammatory mediators ( nfκb , il-1β ). Developmental and behavioral assays revealed stronger protection from NAR pretreatment than post-treatment. Specifically, pretreatment alleviated BMAA-induced defects by restoring muscle architecture, preserving NMJ integrity, normalizing myogenic gene expression, and suppressing inflammatory responses. This study expands the toxicological profile of BMAA to include peripheral neuromuscular structures and identifies NAR as a potential protective agent against environmentally induced neuromuscular toxicity. ● BMAA induces developmental defects and locomotor impairments in zebrafish larvae. ● BMAA disrupts skeletal muscle fibers and neuromuscular junction organization. ● Naringenin pretreatment restores morphology, motor function, and NMJ integrity. ● Naringenin normalizes myogenic gene expression and suppresses inflammation.