Effect of Ovulen and Depo-Provera on primary and secondary immune response in mice and rats.
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Biomedical subjects
Publications and source records attributed to U M Joshi.
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Effects of the administration of PGs A-1, E-2 and F-2 alpha (150 micrograms/rat b.i.d. for 10 days) were studied. Significant increase in testicular weight was observed only in PGE-2 treated group. Testicular ascorbic acid content reduced significantly by treatment with all the PGs. PGE-2 treatment caused a significant decrease in the content of testicular cholesterol, while no change was observed in the same and prostatic acid phosphatase activity in any of the PG treated groups. Blood plasma levels of testosterone drastically reduced by both PGE-2 and PGF-2 alpha, while there was no change in the levels of plasma LH in any of the groups. Plasma FSH levels increased significantly in PGA-1 treated rats only. The results suggest that 1) There is a direct action of PG particularly PGE-2 on testicular weight. PGE-2 increases testicular weight possibly by preventing degeneration of spermatids, 2) PGE-2 acting directly on the testis, reduces testicular ascorbic acid content, stimulates the conversion of cholesterol to pregnenolone but depresses the conversion of the latter to testosterone.
Response of the ovary to ovulation-inducing agents, such as clomiphene citrate and gonadotropin, was assessed using estimations of urinary estrone-3-glucuronide (E1G) by an ELISA test. Baseline data collected over 58 cycles from regularly menstruating women were used as reference. Further, the pattern of E1G excretion was compared with ultrasound assessment of follicular growth. In ovulatory cycles, a good correlation is seen between follicular growth and follicular function. However, when cystic follicles develop after treatment, the correlation is poor: the follicle increases in size without a corresponding increase in E1G excretion. It is suggested that ultrasound examination and hormonal pattern should be used concurrently to assess the response of the ovary to ovulation-inducing agents.
OBJECTIVE: To assess changes in lipoprotein-lipid profile vis-a-vis putative risk of atherosclerotic diseases, among a group of hyperandrogenic women. SUBJECTS AND METHODS: Women studied were among those being screened for polycystic ovarian disease (PCOD) at the Reproductive Endocrinology Clinic of the institute. They all had oligomenorrhea/chronic anovulation as their problem and had clinical or laboratory evidence of hyperandrogenism, viz., hirsutism or elevated serum testosterone levels. Lipoprotein-lipid profiles obtained in 51 such women were compared with those of 11 controls with normal menstrual cycles and no evidence of hyperandrogenism. RESULTS: No significant changes were observed in any of the lipoprotein-lipid variables which could be attributed to hyperandrogenism per se. However, a combined effect of obesity and raised circulating androgens in causing a significant change in the lipoprotein-lipid profile (increased cholesterol, LDL-C/HDL-C, and cholesterol/HDL-C) was clearly discernible from the study. CONCLUSIONS: Hyperandrogenism by itself may not signal a risk for atherosclerotic diseases. However, the potential of such risk would be significantly enhanced if obesity is associated with high circulating levels of androgens.