Neurotoxicity of typical liquid crystal monomers in zebrafish: Disruption of neurotransmitter pathways and underlying mechanisms

The neurotoxicological risks associated with liquid crystal monomers (LCMs), widely used in display technologies, have raised significant ecological and health concerns, yet they remain insufficiently understood. This study systematically investigated three prevalent LCMs – tFPO-CF2-dF3B, 2OdFP3bcH, and TPrCB - for their neurotoxic potential in zebrafish. Exposure to these LCMs induced distinct behavioral impairments, including anxiety-like thigmotaxis and hyper-reactivity to stimuli. At the molecular level, LCMs disrupted key neurotransmitter systems, significantly elevating dopamine, serotonin, and GABA while reducing glutamate. Mechanistic investigation revealed that LCMs bind with high affinity to D2 and 5HT1A receptors via molecular docking, while integrated transcriptomic and neurotransmitter analyses demonstrated concurrent disruption of calcium signaling and mitochondrial function. These findings establish that LCMs induce neurotoxicity through coordinated disruption of multiple neurological pathways, and the identified neurochemical disruptions share features with pathways implicated in human neurological conditions, highlighting the need for rigorous neurotoxic risk assessment of display technology materials and offering important insights for environmental health protection. • Liquid crystal monomers induce anxiety-like behavior and motor deficits in zebrafish larvae. • Liquid crystal monomers disrupt dopamine, serotonin, and glutamate-GABA neurotransmitter systems. • Multi-omics reveal liquid crystal monomers impair synaptic function, ion transport, and trigger neuroinflammation. • Liquid crystal monomers induce neurochemical alterations associated with neurological disorders.