P2.72 Thursday, Jan. 5 Methylmercury uptake and tissue distribution in metamorphosing Xenopus laevis tadpoles fed a swordfish diet ROCK, K.*; GREER, E.; MAYER, M.; SCHREIBER, A.M.; St. Lawrence Univ.; St. Lawrence Univ.; St. Lawrence Univ.; St. Lawrence Univ. email@example.com
Methylmercury (MeHg) is a toxic form of Hg known to bioaccumulate in organisms, particularly in aquatic wildlife. MeHg’s sub-lethal adverse effects include neurotoxicity, endocrine disruption, and immune suppression. Although many studies have measured MeHg levels from wild vertebrates, few controlled laboratory studies on dietary MeHg uptake and tissue distribution have been conducted using amphibian models, partly due to the challenge of effectively administering MeHg. Here we describe a simple and effective method to elevate MeHg loads of lab-raised tadpoles (Niewkoop & Faber stages 54-57) to levels comparable to those found in wetland environments known to contain high MeHg. Tadpoles were raised for 1 month on a diet of powdered swordfish, a top marine predator known to have elevated MeHg content. Compared with controls fed a Pacific salmon diet low in MeHg, pre-metamorphic tadpole (NF 57) tissues were significantly elevated (average tail values: 0.29 vs. 2.20 ppm; average body values: 0.011 vs. 1.570 ppm). Tails from swordfish-fed tadpoles contained almost one-and-one-half times the MeHg concentrations found in the body, likely due to the high muscle content of the tail compared with the body. Interestingly, following either spontaneous metamorphosis or metamorphic induction with exogenous thyroid hormone treatment (30 nM thyroxine, 7 days beginning at NF 57) the concentration of MeHg in the body abruptly doubled, even though the tadpoles were not fed during this period. We attribute the rapid rise in body MeHg levels to transference from the resorbing tail. Therefore, metamorphosis may represent a critical period when tadpoles living in environments containing elevated MeHg are particularly susceptible to its toxic effects.