ABSTRACT The possible role of placental pathology in teratogenesis has not been
fully understood. Since cyclophosphamide is a proven teratogen, it was decided to
investigate its effect on placental histology. A single dose of cyclophosphamide
(20 mg/kg) administered to pregnant rats on day 12 of gestation resulted in various
malformations and stunting of fetuses at term. The placentae were significantly
(P < 0.001) lighter and their margins contained a patch of necrotic substance. The
decidua basalis showed dilatation of blood spaces, hemorrhage and infarction.
Giant cells were numerous and the glycogen cells sparce in the basal zone. Vast
areas of infarction and necrosis were also evident here. The labyrinths were shorter
and often hyalinised. In two cases cysts of considerable size occupied the centre
of the labyrinthine zone. The necrotic patch was found to be fibrinoid in nature
with and without the association of large giant cells and lymphocytes.
ABSTRACT Direct embryotoxic effects of ethanol (EtOH) and acetaldehyde
(AcH) on mouse embryos during early organogenesis were studied using the whole
embryo culture method. Mouse embryos (Jcl-ICR) were cultured for 48 hours
from day 8&1/2 to 10&1/2 (embryonic age; plug day = day 1) with EtOH- or AcHsupplemented
medium. Final concentrations of EtOH ranged from 5 mM to 1 M,
whereas those of AcH ranged from 0.4 pM to 400 mM. Exposure to EtOH at 500
mM or more caused early death. Growth and development in EtOH-exposed embryos
were retarded as indicated by the dose-dependent decrease measured by
several embryonic growth parameters. The most common EtOH-induced anomaly
was exencephaly and it was observed remarkably in the 66 mM or more exposed
group. Exposure to AcH at 40 /.IM or more caused early death. Growth and
development in AcH-treated embryos were retarded as a function of dosage. The
most common AcH-induced anomaly was the deformation complex of the neural
tube such as transparent and prominent rhombencephalon and remarkable shortening
of the posterior part of the body, with or without cyst formation. This deformation
complex was observed remarkably in the 0.8 /.IM or more exposed group.
It can be said by these results that AcH is approximately 10000 times more embryotoxic
than EtOH in the early organogenetic period and both EtOH and AcH
disturb the normal closure of the neural tube, but each compound affects the
closure process in a different way and/or developmental stage.
ABSTRACT This study was undertaken to investigate the morphological relationship
between jaw malformations and developmental disorders of tooth germs in
mouse fetuses following maternal hypervitaminosis A.
Pregnant Slc-ICR mice were treated with a single ip injection of 200001U
vitamin A on day 8, 9 or 10 of pregnancy (VP=O). On days 14-18, they were
sacrificed, and the fetuses were examined for jaw and tooth germ anomalies with
bone-stained specimens and histological sections.
In the group treated on day 8, mandibles were involved with severe reductional
deformities. In the fetuses with defect of the rear portion of the mandibular corpus
and ramus, a pair of incisor-like heterotopic tooth germs were observed behind the
incisors. These abnormal tooth germs had osteodentine in their pulps, and no cusp
was formed. No tooth germ with molar structure was detected. In the fetuses with
less severely deformed jaws, hypoplasia and disarrangement of molars were characteristic.
Significant changes on days 14-1 5 were irregular and excessive epithelial
invaginations from the molar dental laminae.
The tooth anomalies induced by maternal hypervitaminosis A such as incisor-like
heterotopic tooth germs and hypoplastic and disarranged molar germs may have
resulted from spatial derangement of odontogenic mesenchyme due to a deficit of
the embryonic facial mesenchyme.
ABSTRACT We surveyed urogenital anomalies in 119 patients with autosomal
aberrations except Down syndrome. Fifty-three patients had urogenital anomalies.
Horse-shoe kidney occurred in a high frequency in 18 trisomy patients.
Urogenital survey should be recommended to all patients with autosomal anomalies.
ABSTRACT Bis(dichloroacety1)diamine is capable of producing characteristic congenital
malformations in high incidence. Wistar rats were given 200 mg/day of
bis-diamine via a gastric tube on gestation days 9, 10 and 11. The fetuses of 14, 16,
18, 20 days and new born rats were examined using light and electron microscopes
as well as rat T-cell surface markers. The thymus rudiment in rats treated with bisdiamine
has been compared to the normal at each stages.
A high incidence of aplasia or hypoplasia of the thymus was observed in treated
groups. Histological studies of those revealed a short delay in appearance of lymphocytic
cells in the thymus, which initially were blast like and later small lymphocytes,
and also a delay in cortical and medullary differentiation of the thymus.
Immunohistological studies using anti rat T-cell monoclonal antibodies confirmed
the histological findings which show a delay of the development of the thymus.
Bis-diamine induced anomalies were similar to those of the human primary
immunodeficiency syndrome, particularly the DiCeorge syndrome.
ABSTRACT The implausibility of random sampling assumption in experimental
teratology is pointed out. It is emphasized that nonstatistical inference remains a
standard scientific approach, in spite of widespread use of many statistical tests.
The randomization test can be introduced to experimental teratologists as an alternative
to conventional statistical procedures for nonrandom sampling data. A program
list for the randomization test written in BASIC for microcompter is given.