Exogenous iodide ameliorates perchlorate-induced thyroid phenotypes in threespine stickleback.
Perchlorate is a ubiquitous environmental contaminant that has widespread endocrine disrupting effects in vertebrates, including threespine stickleback (Gasterosteus aculeatus). The target of perchlorate is thyroid tissue where it induces changes in the organization, activation, and morphology of thyroid follicles and surrounding tissues. To test the hypothesis that some phenotypes of perchlorate toxicity are not mediated by thyroid hormone, we chronically exposed stickleback beginning at fertilization to perchlorate (10, 30, 100ppm) or control water with and without supplementation of either iodide or thyroxine (T4). Stickleback were sampled across a one-year timespan to identify potential differences in responses to treatment combinations before and after sexual maturation. We found that most thyroid histomorphological phenotypes induced by perchlorate (follicle proliferation, reduced follicle area (adults only), colloid depletion, thyrocyte hypertrophy (subadults only)) were significantly ameliorated by exogenous iodide supplementation. In contrast, treatment with exogenous T4did not correct any of the thyroid-specific histopathologies induced by perchlorate. Whole-body thyroid hormone concentrations were not significantly affected by perchlorate exposure; however, supplementation with iodide and T4significantly increased T4concentrations. This study also revealed an increased erythrocyte area in the thyroid region of perchlorate-exposed adults, while lipid droplet number increased in perchlorate-exposed subadults. Increased erythrocyte area was ameliorated by both iodide and T4, while neither supplement was able to correct lipid droplet number. Our finding on lipid droplets indicates that exposure to perchlorate in early development may have obesogenic effects.
Department of Biological Sciences, University of Alaska Anchorage, Anchorage, AK 99508, USA.
Alison M
AM
Gardell
Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011, USA. Electronic address: Frank.vonHippel@nau.edu.
Frank A
FA
von Hippel
Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011, USA.
Elise M
EM
Adams
Center for Bioengineering Innovation & Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011, USA.
Danielle M
DM
Dillon
Department of Integrative Biology, Oregon State University, Cascades, Bend, OR 97703, USA.
Ann M
AM
Petersen
Institute of Neuroscience, University of Oregon, Eugene, OR 97403, USA.
John H
JH
Postlethwait
Institute of Ecology and Evolution, University of Oregon, Eugene, OR 97403, USA.
William A
WA
Cresko
Center for Bioengineering Innovation & Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011, USA. Electronic address: Loren.Buck@nau.edu.
C Loren
CL
Buck
D000818:Animals; D007454:Iodides / Q000494:pharmacology*; D010472:Perchlorates / Q000633:toxicity*; D010641:Phenotype; D012741:Sexual Maturation / Q000187:drug effects; D023701:Smegmamorpha; D050033:Thyroid Dysgenesis / Q000139:chemically induced / Q000517:prevention & control*; D000072637:Thyroid Epithelial Cells / Q000187:drug effects*; D013961:Thyroid Gland / Q000187:drug effects*; D013974:Thyroxine / Q000494:pharmacology*
D007454:Iodides; D010472:Perchlorates; D013974:Thyroxine; C494474:perchlorate
Endocrine disruption; Histopathology; NIS; Obesogen; Sodium-iodide symporter; Thyroxine