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Stage‐specific effects of defined mixtures of polychlorinated biphenyls on in vitro development of rabbit preimplantation embryos
Author(s) -
Küchenhoff Andreas,
Eckard Rolf,
Buff Klaus,
Fischer Bernd
Publication year - 1999
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/(sici)1098-2795(199910)54:2<126::aid-mrd4>3.0.co;2-b
Subject(s) - embryo , congener , blastocyst , biology , andrology , embryogenesis , in vitro , cell growth , microbiology and biotechnology , biochemistry , chemistry , chromatography , medicine
Abstract PCBs adversely affect various reproductive functions. Little is known about the embryo‐ toxic effects during the preimplantation period in mammals. In the present study the effects of various mixtures of highly purified PCB‐congeners on embryo morphology, blastocyst formation, embryo size and cell proliferation were investigated. For 24 hr, day 3 morulae and day 4 blastocysts were cultured in the presence/absence of coplanar congeners (PCB77, PCB126, and PCB169), non‐coplanar congeners (PCB28, PCB52, PCB101, PCB118, PCB138, PCB153, PCB180) or both mixtures in concentrations ranging from 0.3 ng/mL to 60 μg/mL total PCB. The main effects were (1) degeneration of all embryos at 60 μg/mL, (2) reduction of cell proliferation in day 4 embryos only by coplanar PCB; in day 3 embryos, however, by all PCB‐mixtures, and (3) reduction of cell proliferation in a non‐linear dose response with the strongest impairment caused by the lowest concentration. Cell proliferation was decreased by 0.3 ng/mL coplanar PCB to 50% of the level in control blastocysts. Our results show that purified PCB congeners in the range of 0.3 ng/mL to 30 μg/mL affect the development of preimplantation embryos in a stage‐specific and congener‐specific manner. This study provides first evidence for an embryotoxic potential of coplanar PCB congeners. Mol. Reprod. Dev. 54:126–134, 1999. © 1999 Wiley‐Liss, Inc.