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Developmental stage-dependent carrier effects of nanoplastics on PFOS bioaccumulation and toxicity in zebrafish: Insights from toxicokinetic-toxicodynamic perspective
Summary
Researchers used a toxicokinetic-toxicodynamic framework to study how nanoplastics affect the accumulation and toxicity of the pollutant PFOS in zebrafish at different developmental stages. They found that nanoplastics reduced PFOS uptake in embryos, offering some protection, but significantly increased PFOS accumulation and toxic effects in larvae. The study highlights that nanoplastics can act as either toxicity mitigators or amplifiers depending on the organism's life stage.
The long-term coexistence of nanoplastics (NPs) and persistent pollutants like perfluorooctane sulfonate (PFOS) in aquatic ecosystems necessitates an understanding of their combined effects on organisms across different life stages. Here, a toxicokinetic-toxicodynamic (TK-TD) framework was employed to elucidate life stage-dependent mechanisms of NPs-PFOS interactions in zebrafish. At the embryonic stage (0-48 h), the presence of NPs reduced PFOS accumulation by decreasing its bioavailability, consequently mitigating hatching suppression relative to PFOS exposure alone. Conversely, at the larval stage (72-168 h), combined exposure significantly increased PFOS accumulation and exacerbated multilevel toxic effects, including oxidative stress, metabolic dysregulation, disruption of circadian/visual/nervous pathways, and ultimately behavioral deficits (e.g., abnormal swimming). Using the TK model, we quantified the bioaccumulation kinetics modulated by NPs in zebrafish during the embryonic and larval stages. The Bayesian benchmark dose (BBMD) model based on internal concentration indicated no significant alteration of the PFOS dose-response relationship by NPs, implying that the carrier effect of NPs was the primary mechanism driving life stage-specific outcomes. These findings highlight the necessity of investigating life stage-specific risks for NPs-contaminant co-exposure, where NPs transition from toxicity mitigators in embryos to toxicity amplifiers in larvae mediated by carrier effects, as quantified by the TK-TD perspective.