Janz D M, Bellward G D
Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Toxicol Appl Pharmacol. 1996 Aug;139(2):281-91. doi: 10.1006/taap.1996.0167.
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.
甲状腺激素在禽类围产期的生长和发育中起着重要作用，并且已表明2,3,7,8-四氯二苯并对二恶英（TCDD）及相关化合物会使实验动物体内的这些激素发生改变。由于某些接触TCDD及相关化合物的食鱼鸟类种群繁殖成功率下降的特征是胚胎和幼雏死亡率高，我们研究了在鸡（原鸡）、家鸽（鸽）和大蓝鹭（苍鹭）围产期，胚胎期暴露于TCDD对血浆甲状腺激素浓度（总T3、总T4）以及身体和骨骼生长的影响。肝乙氧基异吩唑酮O-脱乙基酶（EROD）活性也被测定，作为TCDD诱导细胞色素P450IA的酶标志物。在胚胎第4.5天（0.1微克/千克蛋）将[3H]TCDD注入鸡蛋（孵化期21天）的气室，在胚胎第3.5天（1微克/千克蛋）和胚胎第14天（3微克/千克蛋）注入鸽蛋（孵化期18天），在孵化中期（约2微克/千克蛋）注入鹭蛋（孵化期28天）。鸡在胚胎第17天和第19天、出雏日（胚胎第21天）以及出雏后第2天和第4天安乐死。鸽和鹭在出雏时（分别为胚胎第18天和第28天）安乐死，或者在处死前喂食无污染饲料7天。尽管鸡的肝EROD活性比对照组诱导了13至43倍，但TCDD暴露对孵化率、身体生长、皮下水肿或血浆甲状腺激素水平没有影响。在胚胎第3.5天暴露于TCDD的鸽中，EROD诱导了6至15倍，孵化率降低，肝体重比升高，身体和骨骼生长减少（p<0.01）；然而，TCDD暴露对血浆甲状腺激素水平没有影响。同样，在胚胎第14天暴露于TCDD的鸽中，EROD诱导了10至14倍，肝体重比升高，身体和骨骼生长减少（p<0.01），但TCDD处理对血浆甲状腺激素水平没有影响。在鹭中，肝EROD活性比对照鸟诱导了2至3倍，类似于在不列颠哥伦比亚省乔治亚海峡暴露于环境水平的TCDD及相关化学物质的鹭幼雏中测得的EROD活性。然而，这种TCDD暴露水平对鹭的血浆甲状腺激素水平或身体生长没有影响。总体而言，这些结果表明，在鸡、鸽和大蓝鹭的胚胎发育过程中，围产期血浆甲状腺激素水平不能用作TCDD暴露的相对非侵入性生物标志物。
