Seafood safety has evoked worldwide concerns about metal bioaccumulation in marine fish, either in wild or farmed fish. Consumption of wild captured fish is usually a dominant mercury source for humans. Our results showed that mercury bioaccumulation can be influenced by mercury speciation in prey, the presence of Se, and fish body size. Subcellular fractionation of mercury in natural prey distinguished bioavailability of different Hg species. Hg(II) associated with the insoluble fraction was less bioavailable than that in soluble fraction, whereas MeHg in each fraction had comparable bioavailability. Basic biokinetic measurements revealed that Se had direct interaction with Hg(II) during dietary assimilation but not with MeHg, and that different Se species had variable effects on Hg(II...[ Read more ]

Seafood safety has evoked worldwide concerns about metal bioaccumulation in marine fish, either in wild or farmed fish. Consumption of wild captured fish is usually a dominant mercury source for humans. Our results showed that mercury bioaccumulation can be influenced by mercury speciation in prey, the presence of Se, and fish body size. Subcellular fractionation of mercury in natural prey distinguished bioavailability of different Hg species. Hg(II) associated with the insoluble fraction was less bioavailable than that in soluble fraction, whereas MeHg in each fraction had comparable bioavailability. Basic biokinetic measurements revealed that Se had direct interaction with Hg(II) during dietary assimilation but not with MeHg, and that different Se species had variable effects on Hg(II) assimilation. As a result, the presence of Se in prey could reduce Hg(II) accumulation. Hg(II) and MeHg concentrations in field-collected fish were related to 0.19 and 0.33 power of fish size, respectively. Among the examined kinetic parameters, both growth rate and elimination rate constant differences were sufficient to explain most of the size-dependent mercury accumulation.

In addition to mercury bioaccumulation in wild marine fish, the commercial fish diet contaminated by Cd and Cu also pose potential risks to public health. After 28-day exposure to Cd-contaminated diet, hepatic metallothionein (MT) induction and subcellular Cd redistribution suggested that fish suffered from sublethal toxicity from dietary Cd. Likewise, MT induction rather than uptake kinetics modification played a critical role during dissolved Cu acclimation. After quantifying Cu uptake kinetics in marine fish, we further assessed dietary Cu toxicity and unified exposure, accumulation and toxicity from water and food. Influx rate provided a standardized assessment of Cu accumulation in fish tissues and accommodated differential effects from both uptake pathways. Furthermore, gill Cu levels could serve as a good indicator of chronic Cu toxicity, allowing for differences in the relative importance of uptake pathways in different field situations.

To conclude, this study is largely driven by the mounting international concerns about seafood safety, delineating that metal species in the prey, biological factors and exposure routes could greatly affect metal bioaccumulation and consequential toxicity. Compared to the well-known waterborne exposure, this study provides a first step towards the underlying mechanisms of dietary metal accumulation and its toxic effects in marine fish. On one hand, it provides valuable information to help reduce metal levels in marine fish to safety levels for public health, by revealing critical factors controlling metal bioaccumulation. On the other hand, this study indicates that current water quality criteria without consideration of dietary exposure under-protect the aquatic organisms.