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Alcohol as a teratogenic agent inhibits cell growth, function, proliferation and migration by affecting macromolecules, and can induce cell death. Prenatal ethanol exposure causes neural tube defects (NTD) and growth deficiency in experimental animals. NTDs are a group of malformations that result in failure of neural tube (NT) closure in early embryonic development and are among the most common congenital malformations in humans. NTDs are also associated with a number of other central nervous system malformations. Basal layers are the most densely stained structures with Alcian blue which determines glycosaminoglycan (GAG) types. While all sulphated GAGs were observed in the basal layers of NT of the embryos in control and saline-injected groups, hyaluronic acid was dominant in the 10% alcohol-administered embryos. It was reduced in the 15% alcohol-administered embryos and keratan sulphate was significantly low in 20% samples. Especially in the control and saline-injected groups, chondroitin sulphate and dermatan sulphate were highly expressed around cells migrating from the NT, while the same were reduced in 10% alcohol-administered embryos. In 15% alcoholadministered embryos, while the heparine and heparane sulphate were dense around cells migrating from the NT, staining specificities were decreased in 20% alcohol-administered embryos in same regions. Increased alcohol degrees cause decrease of the GAG types in both areas. Key words : Neural tube development, alcohol, glycosaminoglycans (GAGs), chick.

Histochemical determination of glycosaminoglycans (GAGs) in normal and ethanol-induced chick embryo during neural tube development