P-119: Melatonin Protects Folliculogenesis through Up-Regulation of Estrogen Receptors in Mouse under Treatment with Nicotine

Background: Melatonin as the major hormone produced by the pineal gland has a significant role in mammalian reproduction. In this study the efficacy of melatonin coadministration with nicotine on mouse follicogenesis was investigated. Materials and Methods: A total of 32 Female adult NMRI mice were divided into four groups. The control group (n=8) received vehicle, group 2 (n=8) received nicotine (0.4 mg/100 g body weight) for 15 days, group 3 (n=8) was administered melatonin 10 mg/kg for 5 days. Group 4 (n=8) received both nicotine (0.4 mg/100g body weight) and melatonin (10 mg/kg). After autopsy on 16th day, evaluations were made by histopathology, immunohistochemistry methods for evaluation of P53 and estrogen receptor (ER) expression in ovarian follicles and ELISA for serum estradiol level. Statistical analyses were performed by ANOVA. Results: Nicotine significantly reduced the number and size of follicles and estradiol levels compared to the control (p<0.01). While melatonin in group 4 caused a marked normalization in follicogenesis and estradiol levels compared to group 2. There were not significant statistical differences in P53 expression in ovarian follicles in all groups. A significant increase in expression of (ER) were observed in secondary (2/37 ± 1/01 vs. 0.86 ± 0.59) and antral follicles (1.91 ± 1.60 vs. 0.051 ± 0.12) in melatonin treated group compared with controls (p<0.02). Co-administration of nicotine-melatonin in last group increased expression of (ER) in compare with group 2. Conclusion: The results from this study suggest that adverse effects of nicotine on ovary are not dependent to P53 expression. Nicotine reduces serum estradiol level. Administration of melatonin can protect follicogenesis in mouse ovary under treatment with nicotine, partly through up-regulation of estrogen receptors.