Endocrine Abstracts

JOINT1806

Introduction: In mammalian testes, hormones regulate germ cell survival, with Sertoli cells playing a key role in spermatogenesis. Hormonal imbalances can trigger apoptosis, regulated by BCL-2 family proteins, which either inhibit (BCL-2) or promote (BAD, BAK, BAX) cell death. The study aimed to explore the correlation between hormones and these four markers.

Methods: The study included 58 semen and blood samples from 37 infertile men and 21 control patients. The infertile patients were classified into three subgroups: azoospermia (AZO; n=7; median age =35.17 years), oligoasthenospermia/severe oligoasthenospermia (OAS/OASS; n=5; median age =31.40 years), and oligoasthenoteratospermia/severe oligoasthenoteratospermia (OATS/OATSS; n=25; median age =33.84 years). RNA isolation, cDNA synthesis, and qRT-PCR were performed to assess gene expression. Hormone levels (Cortisol, Dehidroepiandrosteron-sulfat, Estradiol, Testosterone, Free Testosterone, Sex Hormone Binding Globuline (SHBG), Follicle-Stimulating Hormone (FSH), Luteinizing Hormone (LH), Prolactin and Inhibin B) were measured in serum samples using the electrochemiluminescence and ELISA detection method according to the manufacturer’s recommendations. Statistical analysis was performed using GraphPad Prism 10.4.1.

Results: The analysis revealed significant correlations between hormone levels and apoptosis markers in male infertility. In the AZO group, E2, FSH, and LH negatively correlated with BCL2 (r=−0.74, r=−0.67, r=−0.62), BAX (r=−0.78, r=−0.69, r=−0.82), and BAK1 (r=−0.73, r=−0.68, r=−0.86), suggesting a role in suppressing both pro-apoptotic and anti-apoptotic pathways. Notably, SHBG showed a strong negative correlation with BAK1 (r=−0.92), while inhibin B positively correlated with BCL2 (r=0.61), indicating its involvement in promoting apoptosis-related pathways while supporting cell survival mechanisms. In the OAS/OASS group, testosterone, free testosterone, and SHBG demonstrated strong positive correlations with BCL2 (r=0.87, r=0.66, r=0.94), BAK1 (r=1.00, r=0.84, r=0.99), and BAX (r=0.94, r=0.96, r=0.91), emphasizing the role of androgenic regulation in apoptosis. The OATS/OATSS and control group, showed only one negative correlation between cortisol and BAK1 (r=−0.50), respectively DHEA-S and BAK1 (r=−0.53).

Conclusion: The findings indicate that hormonal regulation significantly influences apoptosis in male infertility, with AZO and OAS/OASS groups displaying distinct patterns compared to the control and OATS/OATSS groups. These differences indicate disrupted apoptosis regulation, potentially contributing to infertility and further research is needed to uncover underlying mechanisms and develop targeted therapies.