Abstract

Earlier studies have shown that polychlorinated biphenyls (PCB) do not prevent ovulation, fertilization and implantation, but exposure of female mink during gestation caused fetal death. To understand this phenomenon, 30 PCB-exposed female mink and 30 controls were mated or induced to ovulate without fertilization by treatment with gonadotrophin-releasing hormone (GnRH) and correlations were measured between reproductive, morphological and endocrine parameters. The exposure to PCB (Aroclor 1254) started before ovulation. Equal numbers of animals from each group were killed on days 10, 17 and 26 post-coitum or on GnRH-injection days. Plasma concentrations of progesterone, oestradiol-17beta and oestrone sulphate in sampled blood were then measured. Ovaries, uteri and placentae were examined histologically. Compared with controls, exposure to PCB during the reproductive season resulted in significantly smaller uterine glandular diameters before implantation or at the end of the experiment in both mated and GnRH-treated mink. The GnRH treatment increased the sizes of the ovarian corpora lutea and oesterone sulphate 10 days after treatment but the increase in uterine glandular diameter was significant only in GnRH-treated control animals. Both GnRH-treated and mated PCB-exposed groups displayed a peak in oesterone sulphate concentration that was not observed in any of the control groups. Possible actions of PCB are discussed. The observed histological and hormonal changes in the mated PCB-exposed group did not prevent implantation. Exposure to PCB increased fetal mortality. This effect was associated with an effect on placental development.

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