The effects of isonicotinic acid hydrazide on the early chick embryo

Abstract

ABSTRACT Unincubated White Leghorn fertile eggs were injected with isonicotinic acid hydrazide (INH) through a hole in the shell. A control group was injected with normal saline, a second group with INH plus vitamin B6, and a third group was left unopened. INH, in the doses we used, proved to be lethal for more than 50% of the early chick embryos, and also produced important developmental alterations. Alterations produced by INH were primarily observed at the level of the neural epithe-lium, particularly at its cephalic portion. The most important ones were a degenerative and necrotic process of the neural epithelium, and a distortion of the normal anatomical relations of the cephalic structures. The embryonic mortality and developmental alterations induced by INH were prevented to a considerable extent by the concurrent injection of pyridoxine hydrochloride and INH. The preventive action of vitamin B6 suggests that toxicity of INH in the chicken embryos is due to the antivitamin-B6 action of INH. Through this mechanism INH would block, specially, the amino acid metabolism. The developing nervous system was the embryonic area most sensitive to such metabolic alterations.