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Transboundary ecological risks and toxicological mechanisms of a fluorinated liquid crystal monomer and aged microplastics
Summary
Researchers investigated how a fluorinated liquid crystal monomer adsorbs onto and desorbs from aged microplastics under environmental and simulated gastrointestinal conditions, finding that intestinal components remobilize up to 52.8% of the adsorbed contaminant and that the released compound causes mitochondrial dysfunction and oxidative stress-driven apoptosis in gut cells.
Fluorinated liquid crystal monomers (FLCMs) have recently emerged as persistent organic pollutants, while microplastics serve as important environmental carriers of persistent organic pollutants. However, their interactions with aged microplastics and the consequent ecological risks remain a critical blind spot. This study examined the adsorption-desorption dynamics of a representative FLCM (4-ethoxy-2,3-difluoro-4'-(trans-4-propylcyclohexyl) biphenyl, EDPB) on aged polyethylene, polypropylene, polystyrene, and polyvinyl chloride under both abiotic (i.e., environmental) and biotic (i.e., simulated gastrointestinal) conditions. Surface oxidation and increased roughness of aged polymers markedly enhanced EDPB adsorption, through combined hydrophobic attraction and fluorine‑mediated dipole interactions. Desorption was strongly medium dependent. In simulated gastric fluid, pepsin facilitated partial release (12.6-24.8%) by disrupting π-π interactions and promoting surface hydration. In contrast, intestinal components induced substantial remobilization (up to 52.8%) via the formation of hydrophobic cavities and micelle-like structures, increasing dissolved EDPB concentrations by approximately 20 μg L. This biphasic desorption profile highlights the critical role of intestinal processes in remobilizing adsorbed FLCMs and elevating their bioaccessible fractions. Subsequent cytotoxicity assays in Caco‑2 cells showed dose‑ and time‑dependent inhibition of cell viability, with transcriptomic analysis delineating a mitochondrial dysfunction-driven cascade. EDPB acts as a metabolic disruptor that impairs mitochondrial energetics and redox homeostasis, triggering downstream genomic instability and cell cycle arrest, which ultimately implicating oxidative stress-mediated apoptosis. This work synthesizes critical insight into the coupled environmental and biological behaviors of FLCMs, revealing their potential as transboundary persistent toxic substances and advancing the understanding of their risks in microplastic‑dominated systems.
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