Prenatal exposure to high galactose adversely affects initial gonadal pool of germ cells in rats

In rats, prenatal exposure to high concentrations of galactose may contribute to a condition that is equivalent to the premature ovarian failure (POF) component of human galactosaemia. We investigated if development of POF under experimental galactosaemia-like conditions was attributed to impaired germ cell migration. Pregnant rats were fed pellets supplemented with, or without, 35% galactose from day 3 of conception continuing through parturition. Between days 12±15, embryos from one uterine horn were dissected out. Primordial germ cells (PGC) were histochemically localized and counted on the basis of binding of Dolichos bi¯orus agglutinin, a lectin speci®c for terminal N-acetylgalactosamine (GalNAc), to the surface glycoconjugate of the germ cells. The embryos from the other uterine horn were maintained until parturition. Liver activity of uridine diphosphate galactose 4-epimerase, the enzyme involved at multiple steps in the process of synthesis of GalNAc, was assayed in 1±2 day old female pups.The numbers of PGC at the day-speci®c sites on all days of examination were signi ®cantly lower (P < 0.0003), and liver epimerase activity was signi®cantly (P = 0.000001) reduced in the galactoseexposed group.Impaired germ cell migration leading to the development of gonads with de®cient initial pools of germ cells may form the causal link between galactosaemia and POF