In order to evaluate the teratogenic effects of ethylnitrosourea (ENU), a transplacental carcinogen, on the developing central nervous system of the rat embryo. ENU was administered intravenously to pregnant rats on day 9, 12, 14 or 18 of gestation. All malformations induced were specific for the developmental stages. Hydrocephalia was divided into two groups, obstructive and dysgenetic, in relation to developmental mechanism. Micrencephalia associated with hypoplasia of the telencephalon and disorderly arrangement of the lamellar structure in the pallium was produced by treatments on day 12 and day 14. Irregular migration of neuronal cells and cell death caused by the cytotoxic effect are considered to be the developmental mechanisms of micrencephalia. Meningocele, meningoencephalocele, anencephalia and acrania might be a series of malformations which developmental mechanisms were related each other. The relationship of anencephalia or acrania to the development of micro-holoprosencephalia is suggested. Distinctive and common features of these malformations were hypoplastic deformities of the telencephalon .

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Visceral anomalies were studied in two cases of thoracopagus which presented a complex picture. In the first case (female) except for a fused heart and a common liver, both twins had completely independent gastrointestinal tracts along with other normal viscera. In the second case (male), apart from cardiovascular anomalies, a portion of gastrointestinal tract was common to both twins indicating incomplete fission of the yolk sac. One of the twin (B') in this case had only one kidney and one suprarenal while the other twin (A') had these viscera on both sides. These anomalies may be ascribed to the absence of both umbilical arteries in the twin (B') of this case.

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A 4-year-old boy was seen with complaint of penoscrotal hypospadias. The gonadal structures were bilaterally palpable in a normally developed scrotum. The chromosome constitution of 46, XX was established by leukocyte culture. Any female genital ducts could not be demonstrated surgically. The gonads were histologically confirmed to be testis on right side and ovotestis on left side. To our knowledge this is the second case of such phenotypic expression in true hermaphroditism.

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The experimental system for the production of congenital micro- or anophthalmic rats by the treatment of their mothers with CdSO_4 was reported. By the preliminary teratological study, CdSO_4 was shown to be teratogenic when administered to the mother at a dose of 3 mg/kg on gestational day 8, 9 or 10, and of 5 mg/kg on gestational day 7, 8, 9 or 10. The litters from the mothers treated with 3 mg/kg CdSO_4 on gestational day 8 exhibited eye anomalies only, without a significant reduction of the mean fetal body weight compared with control litters. A significant number of offspring from the correspondingly-treated mothers died within I day after birth or during postnatal days 1-30, but a considerable number of the pups with unilateral or bilateral micro- or anophthalmia survived without a significant reduction in the mean body weight compared with the control group. A significant number of bilateral anophthalmic pups associated with hydrocephalus were also obtained, although a large number of them died during postnatal days 1-30. The present experimental system was very suitable for the study of the developmental interrelationship between the neuronal cells in the visual pathway and the eyes.

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Concanavalin A (Con A), which has been shown to bind to carbohydrates on cell surface membranes, was examined for teratogenicity in the mouse. Con A was injected intravenously into pregnant JCL: ICR mice at a single dose of 2.5, 3.0 or 5.0 mg/kg on days 6-13 of pregnancy, and the fetuses were examined on day 18 of pregnancy. Maternal administration of Con A was teratogenic in mice, especially when treated on day 7 of pregnancy. In the groups treated on day 7 of pregnancy, Con A produced malformations such as exencephalia, thoracic vertebral and rib abnormalities. The incidence of exencephalia was dose-dependent. The incidence of skeletal variations was also increased in fetuses by the treatment with 5.0 mg/kg of Con A on day 7 of pregnancy.

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