Although a number of studies in animal models have shown embryolethal
and teratogenic lead effects when this element is administered by a pa
renteral route, the mechanism of the embryonary changes is well not es
tablished. In this study, the embryonic effects of parenteral lead exp
osure on day 9 of gestation were assessed in the Swiss mouse. Lead ace
tate trihydrate was injected intraperitoneally at 14, 28, 56 and 112 m
g/kg. There was no maternal toxicity evidenced by death, reduced body
weight gain or reduced food consumption. However, absolute placental w
eight at 112 mg/kg and relative placental weight at 14, 56 and 112 mg/
kg were diminished significantly. The number of total implants, live a
nd dead fetuses, sex ratio and fetal body weight were unaffected by le
ad exposure. Most sections of placenta showed vascular congestion, an
increase of intracellular spaces and deposits of hyaline material of p
erivascular predominance. Trophoblast hyperplasia was also observed, w
hereas there was a reinforcement of the fibrovascular network in the l
abyrinth. It is concluded that the trophoblast hyperplasia observed in
the placenta of pregnant mice after parenteral lead exposure at doses
that are not toxic for the dam could act as a repairing mechanism of
the extraembryonary tissues. (C) 1996 W. B. Saunders Company Ltd