Environmental pollutants as aetiological agents in female reproductive pathology: placental glycan expression in normal and polychlorinated biphenyl (PCB)-exposed mink (Mustela vison).

Polychlorinated biphenyls (PCB) may cause growth retardation or fetal death in mink. Pathological changes in endotheliochorial mink placentae were examined following exposure to PCB during gestation. Placentae from six animals with average fetal crown-rump (C-R) lengths between 16 and 53 mm given 0.65 mg/day Clophen A50 (low dose), and one from five animals with an average fetal C-R length of 14 mm given 1.3 mg/day (high dose), were examined. Mink were treated from 9 to 24 days before mating until killed at day 53. Placentae were formalin-fixed with four size-matched controls and embedded in resin. Sections were stained with five biotinylated lectins to detect specific glycans. Both control and treated (low dose) mink showed degenerative changes in maternal endothelium from 13-16 mm, revealed by increased lectin binding, caused probably by high cell turnover during tissue remodelling. Controls of 47 and 50 mm exhibited fewer degenerate maternal endothelial cells. The 31-mm PCB-treated tissue showed separation of the trophoblast from the interstitial layer and, at 53 mm, loss of its normal architecture, increased damage to maternal endothelium and infarction. High-dose PCB was extremely toxic, producing fetal death or extensive placental infarction by 14 mm C-R length. Lectin staining thus revealed the effects of PCB toxicity, shown by increased injury to maternal endothelium and severe trophoblastic damage.