[in Japanese]

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The experiment was designed to examine the effect of vitamin E upon the teratogenicity of hypervitaminosis-A in the mouse. Three or five mg of a-tocopherol acetate was administered to the pregnant mice or twice during the period from day 1 to 9 of pregnancy. The hypervitaminosis-A in the pregnant mice was produced by a single administration of 10,000 IU or 15,000 IU of vitamin A on day 10, 11 or 12 of pregnancy. The fetuses from the mothers treated with vitamin A alone and with both vitamin A and vitamin E were examined grossly and in the bone stained specimens on day 19 of pregnancy. The incidences of micromelias were 78-90 % in the groups treated with vitamin A alone. While, the incidence was significantly lower in the group treated with 3mg of a-tocopherol acetate on day 1 and 6 prior to the vitamin A administration, compared to the groups treated with vitamin A alone. This result indicates that vitamin E may play the role of a suppressive effect against the teratogenicity of hypervitaminosis-A. In another series of experiment, the administrations of excess amounts of vitamin A to the pregnant mice caused a decrease of vitamin E content in their livers and a disappearance of vitamin E in the fetuses. This suggests that excess of vitamin A reveals an unfavorable effect on vitamin E metabolism.

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Effects of riboflavine, pyridoxine or folic acid on the incidence of malformations in the Wistar rat fetus caused by maternal hypervitaminosis-A during pregnancy were examined. The hypervitaminosis-A in the pregnant rats was produced by oral administrations of vitamin A at a dose of 30,000 I. U./100g body weight/day from day 10 to day 13 of pregnancy. Riboflavine, pyridoxine or folic acid was administered subcutaneously to the pregnant rats which were treated with vitamin A on the same days of pregnancy. The doses of the above three were 0.05 mg/100 g body weight/day, respectively. 1. The number and the body weight of the live fetuses were significantly greater both in the group treated with vitamin A and pyridoxine (A+p) and the group treated with vitamin A and folic acid (A+F) than in the group treated with vitamin A alone (A). No fetus with growth retardation could be observed in groups A+P and A+F. 2. The growth of the fetal skeleton was examined in the states of ossification of the occipital bones, sternebrae, metacarpal bones, metatarsal bones and cocyges. The ossification in group A+F was much more retarded than that in group A; while, the ossification pattern in groups A+P and A+R was not so much different from that in group A. 3. Among the gross malformations manifested, facial malformations such as microtia, short snout and cleft palate were predominant in each of the experimental groups. The incidences of those malformations in groups A+P and A+F were lower than those in group A; while, the incidence in group A+R was not so different from that in group A. 4. Among the skeletal malformations, the incidence of mandibular malformations was much higher in groups A+F, A+P and A+R than in group A. The malformations of the long bones of extremities were higher in frequency in group A+R, but they were not manifested in groups A+F and A+P. 5. The above results indicated that riboflavine did not suppress the adverse effects of hyparvitaminosis-A upon the fetal development, but folic acid and pyridoxine showed some suppressive effects on the teratogenicity of hypervitaminosis-A when administered at the same time of vitamin A treatment.

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Examinations were carried out on (1) the effect of growth hormone and (2) the combined effect of ethylurethan and growth hormone upon the development of the offspring of primigravid mice of Japanese dd strain. The pregnant mice were divided into four groups as follows: Group I (G. h. Group): 18 pregnant mice were subcutaneously injected on each of days 9, 10 and 11 of gestation with 0.1 % growth hormone solution in physiological saline at the dosage of 0.5 mg/animal. Group II (U Group): 18 pregnant mice were intraperitoneally injected on day 10 of gestation with 10 % ethylurethan aqueous solution at 1.2 mg/g. Group III (G. h. + U Group): 16 pregnant mice were subcutaneously injected on each of days 9, 10 and 11 of gestation with 0.1 % growth hormone solution in physiological saline at 0.5 mg/animal and intraperitoneally treated on day 10 of gestation with 10 % ethylurethan aqueous solution at 1.2 mg/g. Group IV (Untreated Group) : 16 pregnant mice were not treated at all. On day 18 of gestation, all the mothers were sacrificed and the. fetuses were examined macroscopically. The results may be summarized as follows: 1. A significantly higher fetal body weight was seen in the G. h. Group in comparison with those of the Untreated Group, but between the U Group and the G. h. + U Group, the difference of fetal body weight was statistically insignificant. These results mean that growth hormone has some effect in promoting fetal development but does not prevent the retardation of fetal development induced by ethylurethan. 2. There was no significant difference on the fetal mortality between the G.h. Group and the Untreated Group, nor between the U Group and the G. h. + U Group. However, the mortality of fetuses of both the U Group and of the G. h. + U Group was significantly higher than that of the Untreated Group. That is, growth hormone does not influence fetal mortality nor protect against the lethal effect of ethylurethan. 3. No significant difference was seen in the incidence of malformed fetuses between the G. h. Group and the Untreated Group. A teratogenic effect was found in the U Group and the G. h. + U Group, but there is no significant difference between U Group and G. h. + U Group. So, it is indicated that growth hormone does not mitigate the teratogenic effect of ethylurcthan.

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