Smits J E, Bortolotti G R
Toxicology Centre and Veterinary Pathology, University of Saskatchewan, Saskatoon, Canada.
J Toxicol Environ Health A. 2001 Feb 23;62(4):217-26. doi: 10.1080/009841001459388.
Antibody-mediated immune function in adult and recently fledged (30 to 33 d old) American kestrels (Falco sparverius) was examined in birds exposed directly, or only in ovo, to polychlorinated biphenyls (PCBs). In 1998, 9 mature male and 9 female kestrels were fed PCBs, whereas 9 females and 10 males served as controls. A mixture of Aroclors 1248:1254:1260 suspended in safflower oil was injected into the kestrels' food items, while in control diets only the same volume of oil was added. The dosage of PCBs was approximately 7 mg/kg kestrel/d, beginning in March 1998 and continuing for 120 d. In 1998, the antibody-mediated immune response was stimulated by immunization and booster vaccinations of the kestrels using a nonpathogenic antigen, dinitrophenol-keyhole limpet hemocyanin (DNP-KLH). In 1999, offspring from three treatment groups based upon maternal exposure to PCBs were similarly tested for their antibody response. None of these mothers was vaccinated with DNP-KLH the previous year. The maternal groups were: (1) exposed to PCBs in 1998 for 120 d, (2) exposed in ovo in 1998 (i.e., mothers were produced by PCB-exposed parents), or (3) unexposed to PCBs. Serum antibody levels were determined using an enzyme-linked immunosorbent assay (ELISA). In 1998, PCB-exposed adult females had a significantly higher antibody response than did controls, whereas adult males exposed to PCBs had significantly suppressed antibody production. For the nestlings produced in 1999, maternal treatment significantly affected antibody response. Generally, the antibody response in the nestlings was much lower than that seen in adult kestrels. Yet both male and female offspring from mothers that had been fed PCBs the previous year had significantly higher postbooster anti-DNP-KLH titers than control and in ovo-exposed maternal groups, thus mimicking the response seen in the adult females the previous year. These sex-specific responses in PCB-exposed birds provide further evidence of the endocrine-disrupting behavior of PCBs. Both suppression and stimulation of the antibody response are undesirable because this indicates that the immune system is not able to respond normally to challenges by infectious or other disease-causing agents.
在直接接触或仅在胚胎期接触多氯联苯（PCBs）的成年和刚离巢（30至33日龄）的美洲隼（Falco sparverius）中，研究了抗体介导的免疫功能。1998年，给9只成年雄性和9只成年雌性美洲隼投喂多氯联苯，而9只雌性和10只雄性作为对照。将溶解在红花油中的Aroclors 1248:1254:1260混合物注射到美洲隼的食物中，而对照饮食中仅添加相同体积的油。多氯联苯的剂量约为7毫克/千克美洲隼/天，从1998年3月开始，持续120天。1998年，使用非致病性抗原二硝基苯酚-钥孔血蓝蛋白（DNP-KLH）对美洲隼进行免疫和加强免疫，以刺激抗体介导的免疫反应。1999年，对基于母体接触多氯联苯的三个处理组的后代进行了类似的抗体反应测试。这些母亲在前一年均未用DNP-KLH进行疫苗接种。母体组为：（1）1998年接触多氯联苯120天；（2）1998年在胚胎期接触（即母亲由接触多氯联苯的亲代产生）；或（3）未接触多氯联苯。使用酶联免疫吸附测定（ELISA）测定血清抗体水平。1998年，接触多氯联苯的成年雌性的抗体反应明显高于对照组，而接触多氯联苯的成年雄性的抗体产生明显受到抑制。对于1999年出生的雏鸟，母体处理显著影响抗体反应。一般来说，雏鸟的抗体反应远低于成年美洲隼。然而，前一年投喂多氯联苯的母亲所产的雄性和雌性后代在加强免疫后抗DNP-KLH滴度均显著高于对照组和胚胎期接触多氯联苯的母体组，从而模仿了前一年成年雌性的反应。接触多氯联苯的鸟类中的这些性别特异性反应进一步证明了多氯联苯的内分泌干扰行为。抗体反应的抑制和刺激都是不理想的，因为这表明免疫系统无法对传染性或其他致病因子的挑战做出正常反应。
