Abstract:
Intravenously administered Cd was significantly more toxic to
the pregnant rat on the 20th day of gestation than to the young adult,
weanling or old breeder, and caused extensive damage to the liver
and kidneys. The foetal part of the placenta was affected first at
8 h and the whole organ lost its architecture at 20 h.
2+
A single intravenous injection of 1.25 nig Cd^ /kg body weight
between the 9th and 15th day of gestation resulted in hydrocephalus and
other malformations. Cd^+ administration on the 12th day caused a
dose-dependent inhibition of placental Zn^+-transport. At the' teratogenic
dose, Zn^+_transport was inhibited by 75% &nd caused a 33%
reduction in embryonic Zn2+-concentration at 20 h.
2+
The teratogenic dose of Cd inhibited the activity of embryonic
thymidine kinase by about 60% at 4 h and at 20 h the embryonic DNA
concentration was reduced significantly. The activity of the enzyme
isolated from these.embryos was restored by the addition of Zn2+
in vitro. Placental transport of l^C-leucine and -^C-formic acid as
well as the utilization of these precursors in the synthesis of protein
and RNA respectively. were unaffected at least at short times after
administration of Cd^+ . Therefore, the teratogenic effects of Cd2+
may be related to the inhibition of DNA synthesis.
Oral Cd (30 ppm) for 52 weeks did not produce congenital
deformities, but the generation soon died out. Addition of Pb2+
(150 ppm) to this diet caused an even more dramatic effect on the
reproductive performance, but without foetal deformities. Dietary
Pb^+ increased the kidney uptake of Cd2+, but reduced the renal
concentration of Cd2+f associated with discernible renal damage, from
80 to 50 pg/g wet weight.
2+ 2+
Dietary Cd (30 ppm) produced a Zn deficiency in the foetuses
probably by an inhibition of placental Zn2+-transport and led to
a high incidence of foetal deaths and resorptions.
