The effect of hydrazine has been studied on the chick embryos cultivated in vitro by the method devised by New. Hydrazine treated embryos when grown in Pannet-Compton’s saline for 18–20 h at 37.5 ± 1°C showed abnormalities which are predominantly restricted to brain, neural tube, optic vesicles and somites. The differentiation of heart is also affected but to a lesser degree; when subsequently treated with different amino acids, these show a certain degree of specificity. Not all the amino acids which were used are equally effective in bringing about a reversal of the hydrazine-induced malformation. Predominantly affected are the amino acid conversions which depend on transmethylation reactions. Thus the hydrazine-induced abnormalities are effectively reversed by glycine but not by serine, by methionine but not by homocysteine, thus suggesting that the amino acid conversions which are mediated by folic acid are impaired in the hydrazine-treated embryos. From amongst the nucleic acid precursors which are used for the subsequent treatment of hydrazine-treated embryos, thymidine can effectively reverse the inhibitory effects of hydrazine while uridine cannot. Since other precursors such as orotic acid and adenylic acid are not effective in bringing about the reversal, the results obtained by thymidine and uridine can be explained on the basis of a block in normal methylation reactions brought about by hydrazine. Folic acid itself, as well as other related substances such as p-aminobenzoic acid, choline, vitamin B12 and vitamin C are also quite effective in reversing the inhibitory effects of hydrazine. The mode of action of hydrazine is discussed in the light of the possible inhibition of normal one-carbon and methyl group metabolism by a deficiency of folic acid, induced by hydrazine.

Keywords:
Chick morphogenesis, Carcinogenic effect of hydrazine, Mechanism of its action
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© 1974 S. Karger AG, Basel
1974
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