Cellular Growth during Prenatal and Early Postnatal Periods in Progeny of Pyridoxine-deficient Rats

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Abstract
The effects of different levels of dietary pyridoxine (0.5, 1.0 and 8.0 mg/kg diet) fed during growth, pregnancy and lactation in the rat on prenatal and early postnatal cellular development in progeny were studied. Weights of fetuses and most organs of progeny of rats fed the 0.5 mg level were low. Organs in fetuses of the 1.0 mg group also tended to be small. Extending the deficiency period into lactation resulted in significantly lower body weights and weights of all organs studied in progeny of the group fed the 1.0 mg level of the vitamin. The pyridoxine intake of this group did, however, exceed the NRC (1962) recommendation. Progeny of the 0.5 mg group did not survive the lactation period due to the severe vitamin deficit. During the prenatal period, the 0.5 mg level resulted in lower DNA content in thymus and kidneys, in decreased RNA content in liver, heart and brain and in decreased protein content in liver, kidneys and thymus of fetuses. During early postnatal development the 1.0 mg pyridoxine level fed the mother resulted in young with significantly less DNA, RNA and protein in all tissues studied with the exception of DNA content in brain. This was the only parameter that was not significantly affected by the deficiency. The most severe effects of the deficiency were observed in thymus tissue. The results indicated that a maternal pyridoxine deficiency altered cellular growth and development in the organs of progeny during the prenatal period and that the effects became more adverse when the deficiency was extended into the early postnatal period.