The endocrine activity and structure of the murine ovary following irradiation sterilization

Abstract

Femal albino mice were exposed to 350 R of Co�� whole-body gamma irradiation at 50 R per day at four separate periods of development which included the final week of gestation and the first, second and third weeks of post-partum (p.p.) maturation. These were injected with human chorionic gonadotrophin (HCG) at 21 days of age and P³² at 23 days. The animals were sacrificed at 24 days of age and uterine weights and ovarian uptake of P³² were determined as indexes of HCG response. None of the irradiated females had a significant decline in HCG response at this time. However, mice exposed during the first week p.p. showed a significant decline in HCG response using both uterine weight and P³² uptake as criteria at 34 days of age. Mice irradiated during the third week p.p. likewise showed a significant decline in HCG response two weeks later or at 49 days of age. HCG response remained very significantly lower than controls at all times studied from 34 days to 150 days of age. The time of initial decline in HCG rsponse was noted to coincide with the onset of total destruction of ovarian follicles. As long as any active follicles survived, HCG response was approximately normal. In addition to decline in HCG response and destruction of follicles, the estrous cycles of these irradiated females showed market irregularity or usually total interruption. These results were concluded to infer that the ovarian follicles may be essential to normal estrogen secretion induced by HCG as well as required for control of regular estrous cycles. Both irradiated and normal females with and without HCG treatment were injected with tritiated thymidine after which thymidine incorporation was noted by use of autoradiography. Thymidine incorporation (indicating DNA synthesis) by interstitial cells of the sterile ovary was noted in only about 2% of all cells with no effect by HCG. Autoradiograph cell counts of both HCG treated and non-treated normal ovaries showed that about one-third of the follicular cells were labelled. HCG promoted no furhter apparent inclrease in labelling of the follicular cells. The interstitial cells pf the HCG treated normal ovaries had about 10% of their total number labelled in contrast to only 1% labelled in non-HCG treated. These data were interpreted to support the hypothesis that the secondary interstitial cells of the ovary originate from follicular granulosa and theca cells perhaps in part by atresia and that this process is accerlerated by HCG. The uteri of normal HCG treated females showed that numerous cells of the lamina propria had incorporated thymidine. In contrast, sterile HCG treated mice had little thymidine incorporation by the endometrium when compared with controls. This indicated a higher estrogen secretion in the normal mouse that was able to augment uterine DNA synthesis. Several immature females were irradiated at 20 R per day during the first fourteen days of post-partum growth. These animals also showed a decline in HCG response after 34 days of age and interruption of estrous cycles.