PARENT SESSION
Gonadal Function
350
PRENATAL EXPOSURE TO HIGH GALACTOSE IN RAT DEVELOPS OVARIAN RESISTANCE TO GONADOTROPINS POSSIBLY DUE TO PRODUCTION OF SOME ANTI-GONADOTROPINS .
Chakrabarti, Jana1, Bandyopadhyay, Soma1, Pal, Alok1, Goswami, Sourendra2, Kabir, Syed1, 1 2
ABSTRACT- In rat, prenatal exposure to high galactose concentration through a galactose-rich diet produced hypergonadotropic state with delayed puberty and ovarian resistance to the induction of ovulation by exogenous gonadotropins. N-acetylgalactosamine (GalNac) constitutes parts of the monosaccharide residues of the carbohydrate chains of the gonadotropins. Gonadotropins with altered or without N-linked carbohydrate chain loose their biopotency, and also act as an anti-gonadotropins. We observed that prenatal exposure to high galactose concentration adversely affected the activity of epimerase, the enzyme involved in the biosynthesis of GalNac. The present study explores if refractoriness of the ovary to exogenous gonadotropins under experimental galactosemic state was effected through inhibitory influence of endogenous gonadotropins. Pregnant rats were fed commercial pellets supplemented with, or without 35% galactose from day 3 of conception (presence of spermatozoa in vaginal lavage = day 1) continuing through weaning at 21 days of age. The litters who did not exhibit vaginal opening by day 50 of age (the mean day of vaginal opening in control rats was 41 days) were randomly assigned to a daily sc injection of either 150 
g of GnRH-agonist (n = 18), or 150 l of physiological saline (n=21) in 2 equally divided doses for 10 days. A group of 50-55 day old control rats (n = 15) had sc injection of saline for the same duration. All rats were subjected to PMSG-HCG induced superovulation (PMSG: 30 IU at '0' h, HCG: 50 IU at '52' h, and autopsy at '72' h to check the presence of tubal ova). Ovarian response was assessed in terms of presence of oocytes in the oviduct. Eighty-six percent (13/15) of the control rats responded to PMSG-HCG. In the galactose exposed rats without pituitary desensitisation, ovarian response was evidenced in 38% (8/21)(P<0.01 vs. control), but when gonadotropin stimulation was preceded by pituitary desensitization, 72% (13/18) of the rats exhibited the presence of tubal ova, which was statistically comparable to that of the control rats. The present results provide indirect evidence to suggest that ovarian refractoriness to gonadotropins under experimental galactosemic state was atleast partly attributed to some forms of bio-inactive anti-gonadotropins.
KEY WORDS: galactosemia, ovulation, ovarian resitance to gonadotropin