title: Organizational changes to thyroid regulation in Alligator mississippiensis: evidence for predictive adaptive responses.
abstract: During embryonic development, organisms are sensitive to changes in thyroid hormone signaling which can reset the hypothalamic-pituitary-thyroid axis. It has been hypothesized that this developmental programming is a 'predictive adaptive response', a physiological adjustment in accordance with the embryonic environment that will best aid an individual's survival in a similar postnatal environment. When the embryonic environment is a poor predictor of the external environment, the developmental changes are no longer adaptive and can result in disease states. We predicted that endocrine disrupting chemicals (EDCs) and environmentally-based iodide imbalance could lead to developmental changes to the thyroid axis. To explore whether iodide or EDCs could alter developmental programming, we collected American alligator eggs from an estuarine environment with high iodide availability and elevated thyroid-specific EDCs, a freshwater environment contaminated with elevated agriculturally derived EDCs, and a reference freshwater environment. We then incubated them under identical conditions. We examined plasma thyroxine and triiodothyronine concentrations, thyroid gland histology, plasma inorganic iodide, and somatic growth at one week (before external nutrition) and ten months after hatching (on identical diets). Neonates from the estuarine environment were thyrotoxic, expressing follicular cell hyperplasia (p = 0.01) and elevated plasma triiodothyronine concentrations (p = 0.0006) closely tied to plasma iodide concentrations (p = 0.003). Neonates from the freshwater contaminated site were hypothyroid, expressing thyroid follicular cell hyperplasia (p = 0.01) and depressed plasma thyroxine concentrations (p = 0.008). Following a ten month growth period under identical conditions, thyroid histology (hyperplasia p = 0.04; colloid depletion p = 0.01) and somatic growth (body mass p<0.0001; length p = 0.02) remained altered among the contaminated sites. This work supports the hypothesis that embryonic EDC exposure or iodide imbalance could induce adult metabolic disease states, thereby stressing the need to consider the multiple environmental variables present during development.
authors: School of Natural Resources and Environment and Department of Biology, University of Florida, Gainesville, Florida, United States of America. aspboggs@gmail.com
authors: Ashley S P
authors: AS
authors: Boggs
authors: Russell H
authors: RH
authors: Lowers
authors: Jessica A
authors: JA
authors: Cloy-McCoy
authors: Louis J
authors: LJ
authors: Guillette
mesh_terms: D000220:Adaptation, Biological; D000489:Alligators and Crocodiles / Q000254:growth & development / Q000502:physiology*; D000818:Animals; D005431:Florida; D007454:Iodides / Q000097:blood; D045483:Rivers; D013961:Thyroid Gland / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D013963:Thyroid Hormones / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D007454:Iodides; D013963:Thyroid Hormones; D014284:Triiodothyronine; D013974:Thyroxine
references: Crit Rev Toxicol. 2007 Jan-Feb;37(1-2):163-93
references: 17364708
references: Arch Dis Child Fetal Neonatal Ed. 2002 Nov;87(3):F165-71
references: 12390984
references: Environ Health Perspect. 1994 Aug;102(8):680-8
references: 7895709
references: Thyroid Res. 2009 Mar 31;2(1):3
references: 19335881
references: Arch Environ Contam Toxicol. 1999 May;36(4):447-55
references: 10227864
references: Toxicol Sci. 2004 Oct;81(2):309-15
references: 15254343
references: Nutrition. 1997 Sep;13(9):807-13
references: 9290095
references: Environ Monit Assess. 1991 Mar;16(3):277-85
references: 24241940
references: Crit Rev Toxicol. 2007 Jan-Feb;37(1-2):11-53
references: 17364704
references: J Wildl Dis. 1988 Jan;24(1):62-6
references: 3352097
references: Endocrinology. 1982 Mar;110(3):1037-42
references: 6799277
references: Gen Comp Endocrinol. 1997 Aug;107(2):153-65
references: 9245523
references: Comp Biochem Physiol C Toxicol Pharmacol. 2001 Dec;130(4):447-59
references: 11738632
references: Toxicol Sci. 2004 Nov;82(1):106-13
references: 15310858
references: Reproduction. 2004 May;127(5):515-26
references: 15129007
references: Toxicol Pathol. 2001 Mar-Apr;29(2):250-9
references: 11421493
references: Annu Rev Physiol. 2000;62:439-66
references: 10845098
references: J Clin Endocrinol Metab. 2005 Jul;90(7):4094-100
references: 15827096
references: Gen Comp Endocrinol. 1992 Aug;87(2):312-24
references: 1398024
references: Gen Comp Endocrinol. 2011 Dec 1;174(3):362-9
references: 21986089
references: Endocrinology. 1985 Jun;116(6):2246-50
references: 3996311
references: Am J Physiol Endocrinol Metab. 2000 Jul;279(1):E83-7
references: 10893326
references: Mol Cell Endocrinol. 2012 May 6;354(1-2):111-20
references: 22061623
references: Birth Defects Res C Embryo Today. 2011 Mar;93(1):12-8
references: 21425438
references: Thyroid. 2001 May;11(5):493-500
references: 11396708
references: Comp Biochem Physiol A Mol Integr Physiol. 2005 May;141(1):8-14
references: 15894497
references: Endocrinology. 1997 Jun;138(6):2569-76
references: 9165050
references: Toxicol Pathol. 2009 Jun;37(4):415-24
references: 19387088
references: Am J Med. 1974 May;56(5):586-91
references: 4604964
references: Clin Endocrinol (Oxf). 2001 Mar;54(3):365-70
references: 11298089
references: Annu Rev Nutr. 1989;9:201-27
references: 2669870
references: Toxicol Sci. 2005 Dec;88(2):375-83
references: 16120752
references: Diabetologia. 1992 Jul;35(7):595-601
references: 1644236
references: J Clin Endocrinol Metab. 2003 Dec;88(12):5851-7
references: 14671180