MECHANISM OF ASPIRIN-INDUCED NEURAL-TUBE DEFECT IN CHICK-EMBRYO

The effect of acetyl salicylic acid.(aspirin) on neural tube developme nt in chick embryo was studied, using the chick embryo blastoderm mode l. Aspirin was injected in four different doses sub-blastodermally int o fresh embryonated eggs. The role of PGE(1) and PGF(2 alpha). In the defect induced by aspirin on neural tube development in chick embryo w as studied. PGE(1) (5 C mu g) given after aspirin (30 mu g) treatment was found to produce greater defect in development. All the four doses of aspirin used (i.e., 6, 30, 60 and 120 mu g/embryo) produced signif icant changes P < 0.01) in the neural tube development of chick embryo . pre-treatment with PGE(1) did not modify the defect induced by aspir in, whereas pre-treatment with PGF2 alpha prevented neural tube defect s induced by aspirin. It appears that aspirin (in the doses used) affe cts neural tube formation by decreasing PGF(2 alpha) synthesis in chic k embryo blastoderm.