STERILITY DUE TO RADIOACTIVE PHOSPHORUS IN MICE: A STUDY OF OVARIAN COMPENSATORY HYPERTROPHY

The administration of 60 μCi of 32P to pregnant BALB mice induced sterility in the offspring due to destruction of the gonads. The testes presented aspermatogenesis, trophic Leydig cells and normal secondary sex characteristics. The ovaries showed re-absorption of the primary and secondary follicles, absence of ovulation and progressive luteinization of the stroma, as well as atrophy of the uterus and dioestrus. Apart from the alteration in the pituitary feedback mechanism as a result of these gonadal lesions, a direct effect of 32P on the hypothalamic-hypophyseal axis was observed. In these animals the uptake of 32P by the hypothalamus was significantly lower than in normal or castrated controls. The compensatory hypertrophy of the ovary, 1 month after hemi-castration was significantly decreased. The intrarenal grafting of a normal ovary in a 32P-treated host led to lower compensatory hypertrophies than in normal hosts, as determined both 1 and 3 months after grafting. These results were obtained in female and male hosts of 1, 3 and 6 months of age, with transplanted ovaries aged 1, 3 and 6 months respectively. In all the groups, ovarian compensatory hypertrophy was higher in the male than in the female hosts, but the differences between 32P treated and normal hosts were more significant in the females. This difference persisted even when castration of the host was carried out 1 month before grafting of the ovary and when 32P was administered 1 day after removal of the gonads, thus eliminating any secondary effect. It can be concluded that the administration of 32P during foetal life, apart from causing lesions in the gonads, has a direct effect on the hypothalamus with subsequent alteration in the output of gonadotrophins.