Abstract
Even with a galactose (GAL) restricted diet started perinatally galactosemic women frequently manifest primary or secondary amenorrhea with ovarian failure. We postulated that prenatal or early postnatal exposure to excessive GAL and/or its metabolites might be toxic to oocytes or their precursors. Rats received a control or 50% GAL diet during pregnancy and nursing (day 3 of gestation thru 3-4 wks postnatal), or GAL only while nursing. Oocyte number and follicle type was quantitated as described by Pederson & Peters using stained 5 u serial sections of the 3-4 wk. infant ovary. Animals exposed to GAL prenatally plus postnatally had marked reduction in mean total oocyte number compared to controls (2120 ± 410 S.E.M. vs. 8680 ± 964, p<.0001). This was accounted for almost entirely by a reduction in type I (primary) oocytes (1380 ± 336 vs. 7500 ± 818, p <.0001). No significant change was documented in number of preantral or antral follicles. Postnatal GAL caused equally severe growth retardation with or without prenatal GAL (each an ∼ 3X reduction in body, liver, and kidney wt. vs. controls) but postnatal GAL alone produced no reduction in number of total (8400 ± 581) or type I (7280 ± 363) oocytes. In the rat, prenatal exposure to galactose strikingly reduces the number of primary oocytes; the precise timing and mechanism of toxicity now require elucidation. Galactosemic females may acquire ovarian damage in utero if the mother does not receive a galactose-free diet.
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Chen, Y., Mattison, D., Feigenbaum, L. et al. 1198 REDUCTION IN OOCYTE NUMBER FOLLOWING PRENATAL EXPOSURE TO A HIGH GALACTOSE DIET. Pediatr Res 15 (Suppl 4), 642 (1981). https://doi.org/10.1203/00006450-198104001-01224
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DOI: https://doi.org/10.1203/00006450-198104001-01224