Biomagnification of hydrophobic organic compounds (HOCs) increases the eco-environmental risks they pose. Here, we gained mechanistic insights into biomagnification of deuterated polycyclic aromatic hydrocarbons (PAHs-d 10 ) in zebrafish with carefully controlled water (ng L −1 ) by a passive dosing method and dietary exposures using pre-exposed Daphnia magna and fish food. A new bioaccumulation kinetic model for fish was established to take into account discrete dietary uptake, while the frequently used model regards dietary uptake as a continuous process. We found that when freely dissolved concentrations of the PAHs-d 10 were constant in water, the intake amount of the PAHs-d 10 played an important role in affecting their steadystate concentrations in zebrafish, and there was a peak concentration in zebrafish after each dietary uptake. Moreover, considering the randomness of predation, the Monte Carlo simulation results showed that the probabilities of biomagnification of the PAHs-d 10 in zebrafish increased with their dietary uptake amount and frequency. This study indicates that in addition to the well-known lipid−water partitioning, the bioaccumulation of HOCs in fish is also a discontinuous kinetic process caused by the fluctuation of HOC concentration in the gastrointestinal tract as a result of the discrete food ingestion. The discontinuity and randomness of dietary uptake can partly explain the differences among aquatic ecosystems with respect to biomagnification for species at similar trophic levels and provides new insight for future analysis of experimental and field bioaccumulation data for fish.
In the present study, we developed a multicompartmental toxicokinetic model for two polycyclic aromatic hydrocarbons (phenanthrene and anthracene) in their deuterated form (PAHs-d 10) in zebrafish considering continuous waterborne uptake and discrete dietary uptake. We quantified the bioconcentration, bioaccumulation, and depuration of these two PAHs-d 10 in zebrafish, and then estimated the kinetic parameters by fitting the model into the experimental data. The experimental and fitting results both showed that there was a peak concentration in each compartment of zebrafish after every dietary uptake, while the peak value depended on the ingestion amount of the PAH-d 10 and varied among different compartments. The PAH-d 10 amount in the blood reached 20–27% of the total amount bioaccumulated in zebrafish at steady-state, followed by skin (20–26%), and fillet (16–22%). The rank of PAH-d 10 steady-state concentrations in each compartment showed inconsistency with its lipid contents, indicating that the distribution of the PAHs-d 10 in zebrafish was not merely affected by the lipid content in each compartment, but also affected by their kinetics and biotransformation. This study suggests that discrete dietary uptake caused by intermittent food ingestion significantly affects the bioaccumulation of PAHs in fish. Further studies are needed to investigate such effect on other toxicants that are more resistant to biotransformation than PAHs in fish.
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