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Human Reproduction, Vol. 18, No. 2, 276-282, February 2003
© 2003 European Society of Human Reproduction and Embryology

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

S. Bandyopadhyay1, J. Chakrabarti1, S. Banerjee2, A.K. Pal1, D. Bhattacharyya3, S.K. Goswami2, B.N. Chakravarty2 and S.N. Kabir1,4

1 Reproductive Biology Research, Indian Institute of Chemical Biology, Jadavpur, Kolkata 700032, 2 Institute of Reproductive Medicine, Salt lake, Kolkata 700091 and 3 Division of Protein Engineering, Indian Institute of Chemical Biology, Jadavpur, Kolkata 700032, West Bengal, India

4 To whom correspondence should be addressed. e-mail: snkabir{at}iicb.res.in

BACKGROUND: 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. METHODS: 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 biflorus agglutinin, a lectin specific 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. RESULTS: The numbers of PGC at the day-specific sites on all days of examination were significantly lower (P <= 0.0003), and liver epimerase activity was significantly (P = 0.000001) reduced in the galactose-exposed group. CONCLUSION: Impaired germ cell migration leading to the development of gonads with deficient initial pools of germ cells may form the causal link between galactosaemia and POF.

Key words: galactosaemia/germ cell migration/premature ovarian failure/resistant ovary syndrome

* This communication was presented in part at the 16th Annual Meeting of European Society of Human Reproduction and Embryology, Bologna, Italy, 2000 and 34th Annual Meeting of Society for the Study of Reproduction, Ottawa, Canada, 2001


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