Experimental galactose toxicity may serve as a model for exploring some of the basic tenets of POF.

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.

The effects of pelvic endometrial implants on the overall reproductive potential of female rats were investigated. After homologous transplantation in the peritoneum, the ectopic endometrium developed into highly vascularized nodes that gradually increased in mass until the 9th week postsurgery and then plateaued. In the presence of these implants, overall reproductive function was adversely affected. The effect was of greatest magnitude during 50-70 days posttransplantation. As compared with values in corresponding controls, ovulation was reduced by 43% (6 of 14) (p < 0.05), mating rate was reduced by 44% (12 of 27) (p < 0.025), and premature termination of pregnancy occurred in 34% (5 of 15) of rats. Wastage of pregnancy, which included complete termination or reduction of fetal number, occurred during the postimplantation course of gestation. Furthermore, 100% of the rats with transplants failed to respond to the copulomimetic stimulation for the induction of pseudopregnancy (p < 0.01, compared with corresponding controls). However, on exposure to vasectomized males, 46% (6 of 13) of these rats exhibited development of pseudopregnancy (p < 0.05, compared with corresponding group receiving copulomimetic stimulation). Increased rate of mating failure and differential pseudopregnancy rates after copulomimetic and natural cervical stimulation suggest that the rats with endometrial explants possibly had an absence or a short appearance of behavioral estrus. Hormonal assessment during the preovulatory phase showed a tendency toward lower mean levels of preovulatory estradiol and significantly lower LH (p < 0.01) and progesterone (p < 0.01) concentrations. The adversely affected reproductive functions may be a secondary consequence of these altered endocrine milieus.

No abstract

The precise cellular mechanism of primordial germ cell (PGC) migration remains unknown. Cell surface galactosyltransferase (GalTase) is known to play unique roles in the process of locomotion of many migratory cells. With an objective to seek evidence for possible involvement of GalTase in the migratory process of PGC, we evaluated germ cell migration in the rat following experimental modulation of embryonic GalTase activity. Pregnant rats were laparotomized under anesthesia on Day 10 of pregnancy. While embryos of one uterine horn received lysozyme (100 microg/fetus), those of the other received alpha-lactalbumin (LA; 100 microg/fetus), N-acetylglucosamine (GlcNAc; 250 nmole/fetus), uridine 5'-monophosphate (UMP; 2.5 micromole/fetus), uridine diphosphate-galactose (UDP-gal; 250 nmole/fetus), or a combination of 250 nmole of UDP-gal and 2.5 micromole of UMP/fetus. Between gestation Days 12 and 14, embryos were dissected out and processed for histochemical localization of PGC on the basis of binding of Dolichos biflorus agglutinin on the surface glycoconjugate of the germ cells. The number of PGC in each embryo was counted. There was a daywise increase in the number of PGC in all groups. As compared with lysozyme-exposed controls, the numbers of PGCs at the day-specific sites on all days of examination were significantly lower in the LA- as well as GlcNAc-exposed groups. UMP or UDP-gal individually exerted little or no influence, while the total PGC count rose significantly over the respective control values under simultaneous exposure to UMP and UDP-gal. The present findings suggest a likely catalytic role of GalTase in the process of germ cell migration.