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Inhibition of Xenobiotics Transporters’ Efflux Ability after Nanoplastics Exposure in Larval Japanese Medaka
Summary
Nanoplastics exposure in larval Japanese medaka fish disrupted the efflux activity of ATP-binding cassette transporters, which normally protect cells by pumping out xenobiotics and toxins. The finding suggests that nanoplastics can impair a key cellular defense mechanism in fish, potentially increasing vulnerability to co-occurring chemical pollutants.
Nanoplastics can enter into the aquatic environment as primary nano-sized or fragmented from larger-sized plastic particles, and their ecological effects and environmental fate have aroused increasing public concerns. Here, we identified the disruption of ATP-binding cassette (ABC) efflux after polystyrene (PS) nanoplastics (76 ± 7 nm) exposure in larval Japanese medaka (Oryzias latipes). Nanoplastics (0.001–10 μg/mL) caused 3–6-fold higher lipid peroxidation in fish larvae than the control, with concomitant downregulated expression of efflux transporter-related genes (abcb6a, abcc2, abcg2). Two probes of rhodamine (indicative of p-glycoprotein function for parent compounds’ efflux, P-gp) and fluorescein (indicative of multidrug resistance-associated protein function for metabolites’ efflux, MRP) were further used to verify the inhibited ABC efflux ability, via rhodamine and fluorescein bioaccumulation results. Three-fold higher accumulation of rhodamine was observed following treatment with 10 μg/mL of nanoplastics. Excessive accumulation also occurred for fluorescein, with 1.7–1.8-fold higher concentrations than controls in larvae treated with 0.01–0.1 μg/mL of nanoplastics. Although the inhibition of ABC transporters diminished after two hours of depuration, the co-existence of nanoplastics and other contaminants still raises concerns. Collectively, this study suggests that nanoplastics can negatively impact ABC transporters’ efflux ability and could cause unanticipated accumulation of co-existing organic pollutants in aquatic organisms.
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