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Human reproduction (Oxford, England) · 2003

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

СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bandyopadhyay S, Chakrabarti J, Banerjee S, Pal A K, Bhattacharyya D, Goswami S K, Chakravarty B N, Kabir S N

Аннотация

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.

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