Favour Ayomide Akinpelu, Oluwapelumi Lydia Apanisile, Babatunde Mobolaji Oguntimilehin, Edidiong Nnamso Akang
JBRA Assist. Reprod. 2025; 29 (4):601-607
Received March 31, 2025
Accepted November 19, 2025
Abstract
ABSTRACT
Background: Hormonal contraceptives are widely used to alter the hypothalamic-pituitary-gonadal (HPG) axis, inhibiting ovulation, and altering reproductive hormone levels. Understanding their effects on estrous cycle regulation and fecundity in animal models is essential for evaluating their contraceptive mechanisms and long-term reproductive impact.
Objective: This study aims to investigate the effects of Levonorgestrel and Depot-Medroxyprogesterone Acetate (DMPA) on estrous cycle phases, hormonal disruptions, and fecundity in rodent models, providing insights into their contraceptive efficacy and potential reproductive consequences.
Methods: Fifteen adults female Wistar rats were divided into three groups: Control (water only), Levonorgestrel-treated (0.7 mL oral administration), and DMPA-treated (0.02 mL intramuscular injection). Vaginal cytology was used to track estrous cycle phases before, during, and after treatment. Mating success and fecundity were assessed by pairing treated females with males and recording pregnancy rates and litter sizes.
Results: Both Levonorgestrel and DMPA significantly disrupted estrous cycle regularity. The estrus phase duration was notably shortened in treated groups, while the diestrus phase was prolonged, especially in the DMPA group (P < 0.0001). Mating success was significantly reduced, with only 40% of DMPA-treated and 60% of Levonorgestrel-treated females mating successfully, compared to 100% in the control group. Litter numbers were also significantly lower in treated groups compared to controls.
Conclusion: These findings suggest that prolonged use of Levonorgestrel or DMPA may significantly alter the oestrous cycle, potentially impairing fertility and delaying reproductive recovery. Further studies are needed to explore the long-term consequences of contraceptive-induced cycle disruptions.