title: Maintaining tissue selenium species distribution as a potential defense mechanism against methylmercury toxicity in juvenile white sturgeon (Acipenser transmontanus).
abstract: Selenium (Se) has been shown to antagonize mercury (Hg) toxicity. We have previously demonstrated that orally intubated selenomethionine (SeMet) and methylmercury (MeHg) reduced tissue Se accumulation, as well as blood and kidney Hg concentrations in juvenile white sturgeon (Acipenser transmontanus). However, the form of Se accumulated is not known. In this study, three organoseleniums: selenocysteine (Sec), Se-methyl-selenocysteine (MSeCys), and SeMet and two inorganic Se species: selenate and selenite were determined and quantified in the blood at different post-intubation periods (12, 24, 48h) and in the muscle, liver, and kidneys at 48h in white sturgeon orally intubated with a single dose of control (carrier), SeMet (500μg Se/kg body weight; BW), MeHg (850μg Hg/kg BW), and both (Se+Hg; at 500μg Se/kg and 850μg Hg/kg BW). When only SeMet was intubated, the accumulative/unmodified pathway took precedent in the blood, white muscle, liver, and kidneys. In the presence of MeHg, however, active metabolic transformation and de novo synthesis of biologically active Se forms are seen in the liver and kidneys, as indicated by a gradual increase in blood Sec:SeMet ratios and Se metabolites. In the white muscle, mobilization of endogenous Se storage by MeHg is supported by the absence of tissue SeMet and detectable levels of blood SeMet. In contrast, co-intubation with SeMet increased muscle SeMet. The high levels of unknown Se metabolites and detectable levels of selenite in the kidney reflect its role as the major excretory organ for Se. Selenium metabolism is highly regulated in the kidneys, as Se speciation was not affected by MeHg or by its co-intubation with SeMet. In the Se+Hg group, the proportion of SeMet in the liver has decreased to nearly 1/8th of that of the SeMet only group, resulting in a more similar selenocompound distribution profile to that of the MeHg only group. This is likely due to the increased need for Se metabolites necessary for MeHg demethylation in the liver. Our study demonstrated that in the presence of MeHg, regulating tissue Se speciation, hence, Se bioavailability, is more an important strategy than maintaining total Se levels in major organs of juvenile white sturgeon.
authors.affiliation: Centre for Advanced Research in Environmental Genomics, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5.
authors.forename: Susie Shih-Yin
authors.initials: SS
authors.lastname: Huang
authors.affiliation: Department of Animal Science, University of California, Davis, CA 95616, USA.
authors.forename: Silas S O
authors.initials: SS
authors.lastname: Hung
authors.affiliation: Centre for Advanced Research in Environmental Genomics, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5. Electronic address: laurie.chan@uottawa.ca.
authors.forename: Hing Man
authors.initials: HM
authors.lastname: Chan
mesh_terms: D000818:Animals; D005399:Fishes / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008628:Mercury / Q000378:metabolism; D008767:Methylmercury Compounds / Q000633:toxicity*; D012643:Selenium / Q000378:metabolism*; D018036:Selenium Compounds / Q000378:metabolism*; D017279:Selenocysteine / Q000031:analogs & derivatives / Q000378:metabolism; D012645:Selenomethionine / Q000378:metabolism; D014018:Tissue Distribution; D014874:Water Pollutants, Chemical / Q000378:metabolism / Q000633:toxicity
chemical_list: D008767:Methylmercury Compounds; D018036:Selenium Compounds; D014874:Water Pollutants, Chemical; D017279:Selenocysteine; D012645:Selenomethionine; D008628:Mercury; D012643:Selenium; C002979:selenomethylselenocysteine
keywords: Methylmercury; Se bioavailability; Se metabolism; Se speciation; Selenocompounds; Selenomethionine