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PubMed1952

THYROID hormone.

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Hormones↗
PubMed1996

In ovo 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure in three avian species. 1. Effects on thyroid hormones and growth during the perinatal period.

Thyroid hormones are important in the perinatal growth and development of avian species, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds have been shown to cause alterations in these hormones in laboratory animals. Since the decreased reproductive success in certain fish-eating bird populations exposed to TCDD and related compounds is characterized by high embryo and hatchling mortality, we examined the effects of in ovo TCDD exposure on plasma thyroid hormone concentrations (total T3, total T4) and body and skeletal growth during the perinatal period in the domestic chicken (Gallus gallus), domestic pigeon (Columba livia), and great blue heron (Ardea herodias). Hepatic ethoxyresorufin O-deethylase (EROD) activity was also determined as an enzymatic marker of cytochrome P450IA induction by TCDD. [3H]TCDD was injected into the air cell of chicken eggs (21-day incubation period) on Embryonic Day 4.5 (0.1 microgram/kg egg), pigeon eggs (18-day incubation period) on Embryonic Day 3.5 (1 microgram/kg egg) and Embryonic Day 14 (3 microgram/kg egg), and heron eggs (28-day incubation period) at approximately the midpoint of incubation (2 microgram/kg egg). Chickens were euthanized on Embryonic Days 17 and 19, day of hatch (Embryonic Day 21), and Days 2 and 4 after hatch. Pigeons and herons were euthanized either at hatch (Embryonic Days 18 and 28, respectively), or fed an uncontaminated diet for 7 days prior to sacrifice. Although hepatic EROD activity was induced 13- to 43-fold above controls in chickens, there was no effect of TCDD exposure on hatchability, body growth, subcutaneous edema, or plasma thyroid hormone levels. In pigeons exposed to TCDD on Embryonic Day 3.5, EROD was induced 6- to 15-fold, hatchability was decreased, liver to body weight ratio was elevated, and body and skeletal growth were decreased (p < 0.01); however, there was no effect of TCDD exposure on plasma thyroid hormone levels. Similarly, in pigeons exposed to TCDD on Embryonic Day 14, EROD was induced 10- to 14-fold, liver to body weight ratio was elevated, and body and skeletal growth were decreased (p < 0.01), but there was no effect of TCDD treatment on plasma thyroid hormone levels. In herons, hepatic EROD activity was induced 2- to 3-fold above control birds, similar to EROD activities measured in heron hatchlings exposed to environmental levels of TCDD and related chemicals in the Strait of Georgia, British Columbia. However, this level of TCDD exposure had no effect on plasma thyroid hormone levels or body growth in herons. Collectively, these results suggest that perinatal plasma thyroid hormone levels cannot be used as relatively noninvasive biomarkers of TCDD exposure during embryonic development in chickens, pigeons, and great blue herons.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Hyperactivity and learning deficits in transgenic mice bearing a human mutant thyroid hormone beta1 receptor gene.

Resistance to thyroid hormone (RTH) is a human syndrome mapped to the thyroid receptor beta (TRbeta) gene on chromosome 3, representing a mutation of the ligand-binding domain of the TRbeta gene. The syndrome is characterized by reduced tissue responsiveness to thyroid hormone and elevated serum levels of thyroid hormones. A common behavioral phenotype associated with RTH is attention deficit hyperactivity disorder (ADHD). To test the hypothesis that RTH produces attention deficits and/or hyperactivity, transgenic mice expressing a mutant TRbeta gene were generated. The present experiment tested RTH transgenic mice from the PV kindred on behavioral tasks relevant to the primary features of ADHD: hyperactivity, sustained attention (vigilance), learning, and impulsivity. Male transgenic mice showed elevated locomotor activity in an open field compared to male wild-type littermate controls. Both male and female transgenic mice exhibited impaired learning of an autoshaping task, compared to wild-type controls. On a vigilance task in an operant chamber, there were no differences between transgenics and controls on the proportion of hits, response latency, or duration of stimulus tolerated. On an operant go/no-go task measuring sustained attention and impulsivity, there were no differences between controls and transgenics. These results indicate that transgenic mice bearing a mutant human TRbeta gene demonstrate several behavioral characteristics of ADHD and may serve a valuable heuristic role in elucidating possible candidate genes in converging pathways for other causes of ADHD.

Animals↗