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):292-300. doi: 10.1006/taap.1996.0168.
As opposed to mammals, the heterogametic sex in birds is female, and sexual differentiation of the central nervous system away from the intrinsic male pattern is dependent on ovarian estrogen secretions during the perinatal period. The contamination of aquatic systems with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds has been suggested to be responsible for decreased reproductive success in certain wild fish-eating bird populations. Since TCDD has been shown to alter estrogenic status in laboratory animals, we determined the effects of in ovo TCDD exposure on hepatic estrogen receptor (ER) concentrations and affinities, and plasma estradiol concentrations during the perinatal period in the domestic chicken (Gallus gallus), domestic pigeon (Columba livia), and great blue heron (Ardea herodias). Plasma testosterone levels were also determined in herons as an indication of androgenic status. [3H]TCDD was injected into the air cell of chicken eggs on Embryonic Day 4.5 (0.1 microgram/kg egg), pigeon eggs on Embryonic Day 3.5 (1 microgram/kg egg) and Embryonic Day 14 (3 micrograms/kg egg), and heron eggs at approximately Embryonic Day 13 (2 micrograms/kg egg). Chickens were euthanized on Embryonic Days 17 and 19, hatch, and Days 2 and 4 after hatch. Pigeons and herons were either euthanized at hatch or fed an uncontaminated diet for 7 days prior to termination. Between 5 and 10% of the injected [3H]TCDD dose was measured in the liver of hatchlings. There was no effect of in ovo TCDD exposure on hepatic ER levels or plasma estradiol concentrations in female chickens and pigeons exposed early in incubation. In female pigeons exposed during the latter third part of incubation to a TCDD dose that would cause high embryo lethality if injected early in incubation, hepatic ER concentrations were elevated (p < 0.001) and plasma estradiol concentrations were decreased (p < 0.01) at hatch. There was no effect of TCDD exposure on plasma estradiol levels in male pigeons. In herons, TCDD exposure had no effect on hepatic ER levels or plasma estradiol and testosterone concentrations at either time point. We conclude that in chicken, pigeon, and great blue heron hatchlings exposed early in incubation to low doses of TCDD, hepatic ER levels and plasma estradiol concentrations are not biomarkers of toxicity.
与哺乳动物不同，鸟类中的异配性别是雌性，中枢神经系统从固有雄性模式的性分化依赖于围产期卵巢雌激素的分泌。有人认为，水生系统被2,3,7,8-四氯二苯并对二恶英（TCDD）及相关化合物污染是某些以野生鱼类为食的鸟类种群繁殖成功率下降的原因。由于已证明TCDD会改变实验动物的雌激素状态，我们测定了在鸡蛋、鸽蛋和大蓝鹭蛋中进行TCDD胚胎期暴露对家鸡（原鸡）、家鸽（鸽）和大蓝鹭围产期肝脏雌激素受体（ER）浓度和亲和力以及血浆雌二醇浓度的影响。还测定了鹭的血浆睾酮水平以作为雄激素状态的指标。在胚胎第4.5天向鸡蛋的气室注射[3H]TCDD（0.1微克/千克蛋），在胚胎第3.5天和第14天向鸽蛋注射（分别为1微克/千克蛋和3微克/千克蛋），在大约胚胎第13天向鹭蛋注射（2微克/千克蛋）。家鸡在胚胎第17天、第19天、出壳时以及出壳后第2天和第4天安乐死。鸽和鹭在出壳时安乐死，或者在处死前喂食未受污染的饲料7天。在幼雏肝脏中检测到注射剂量的[3H]TCDD的5%至10%。在孵化早期暴露于TCDD的雌性家鸡和鸽中，胚胎期TCDD暴露对肝脏ER水平或血浆雌二醇浓度没有影响。在孵化后期三分之一阶段暴露于TCDD剂量（如果在孵化早期注射会导致高胚胎致死率）的雌性鸽中，出壳时肝脏ER浓度升高（p<0.001），血浆雌二醇浓度降低（p<0.01）。TCDD暴露对雄性鸽的血浆雌二醇水平没有影响。在鹭中，TCDD暴露在两个时间点对肝脏ER水平、血浆雌二醇和睾酮浓度均无影响。我们得出结论，在孵化早期暴露于低剂量TCDD的家鸡、鸽和大蓝鹭幼雏中，肝脏ER水平和血浆雌二醇浓度不是毒性生物标志物。
