F. Shinku, M. A. Wazhi, V. E. Odey, P. Nyango, M. B. Mohammed, C. N. Edeh, N. Z. Nden, S. S. Gotom, J. S. Kumbet, S. A. Adamu, N. J. Chuwang, Y. M. Usman, M. O. Omolara, R.J. Kutshik, R.T. Mcneil
Serum hormonal profiling via Enzyme-Linked Immunosorbent Assay (ELISA) demonstrated that while CC elevated gonadotropin output via central receptor blockade, high-dose RC and exogenous estrogen generated conflicting biochemical feedback loops that significantly suppressed Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) surges, blocking the pre-ovulatory stimulus. Histological analysis via Hematoxylin and Eosin (H&E) staining showed that exogenous estrogen induced significant Estrogen Receptor Alpha (ERα)-mediated hyperproliferation in the uterine lumen and glandular epithelium, whereas CC caused anti-estrogenic endometrial thinning and glandular atrophy. Conversely, RC extract limited uterine hyperproliferation while maintaining structural boundaries. Ovarian morphometry revealed that RC extract induced marked follicular atresia and a significant reduction in active corpora lutea, establishing a clear anti-fertility footprint. Immunohistochemical (IHC) mapping via semi-quantitative scoring confirmed that RC extract altered the crucial ERα to Estrogen Receptor Beta (ERβ) expression within both endometrial and ovarian granulosa compartments, operating similarly to a Selective Estrogen Receptor Modulator (SERM). These results provide a robust, evidence-based toxicological link validating the traditional empirical use of Ricinus communis as a primitive contraceptive agent.