This study was undertaken to determine whether the administration of vitamins, especially folinic acid (FA) prevent the spontaneous CL/CP or not and to clarify its mechanism. FA was administered to pregnant A/J mice by intraperitoneal injection at 11: 00 A. M. on day 10 of gestation (Plug day = 0) at various doses (3,10,20,30,100, and 300 mg/kg body weight). All pregnant animals were sacrificed on day 18 or 19 of gestation. The number of resorptions and live or dead fetuses were noted. Each live fetus was examined for the presence of CL/CP.
Consequently, cell death of primary palate was investigated using supra vital Nile blue sulphate (NBS)staining on days 10,11, and 12 of gestation.
1. The number of intrauterine m ortality did not increase.
2. The mean incidence of fetus with CLP (especia l ly UCLP) decreased by administering 10 to 30mg/kg body weight of FA to dams on day 10 of gestation.
3. The mean incidence of fetus with CP increased by administering 10 to 30 mg/kg body weight of FA to dams on day 10 of gestation.
4. The mean incidence of fetus with CL/CP did not change.
5. The development stage of the face, the degree and extent of uptaking of NBS in primary palate did not alter between the embryos from a litter that received a dose of FA of 10 mg/kg body weight on day 10 of gestation and from the control litter.
6. Embryos with a potential CL could be found at the crescent stage by asymmetric nasal pit. Embryos with a definite CL could be found at the comma stage by failure of fusion between medial nasal process (MNP) and lateral nasal process (LNP) because MNP were more prominent, and more medially placed.
7. Cell death could be observed in the presumptive fusion zone of normal embryos, and it could be kept in the same areas of the CL fetuses.
8. Administration of FA prevents CL and alter CLP to CP only.
9. The mechanism of prevention of CLP is considered to be FA which does not alter the potentiality of fusion in the presumptive fusion zone, but alters the development of the nasal processes.
10. It is supposed that CP is not isolated congenital malformation from CLP in A/J mice, and the degree of cleft could be due to environmental factors.
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