Impact of fluoxetine on testosterone levels and spermatogenic cell production of male albino mice
نویسندگان
1 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
2 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
3 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
4 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
5 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
6 Faculty of Veterinary Medicine, Non-profit JSC Kazakh National Agrarian Research University, Almaty City, Republic of Kazakhstan
7 Zhangir Khan NJSC «West Kazakhstan Agrarian and Technical University Named after Zhangir khan», Higher School of Veterinary and Biological Safety, Uralsk City, Republic of Kazakhstаn
8 Department of Veterinary Medicine and Technosphere Safety of Engineering Humanitarian Faculty of West Kazakhstan Innovative and Technological University, Uralsk City, Republic of Kazakhstаn
9 Candidate of Veterinary Sciences, Senior Researcher Kazakh Research Veterinary Institute LLP, Almaty city, Republic of Kazakhstan
doi
10.22124/cjes.2023.7401چکیده
Fluoxetine is a widely used antidepressant that acts as a selective serotonin reuptake inhibitor. This study investigated the effects of fluoxetine hydrochloride on the hypothalamic-pituitary-testicular axis and spermatogenesis in male albino mice. Fifty mice were divided into five distinct groups, comprising a control group, an observation group and three separate experimental cohorts receiving oral fluoxetine at doses of 50, 100, and 150 mg kg-1 for 28 days. Testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay. Testicular tissue was analyzed for changes in seminiferous tubule sperm count and spermatogenic cell populations. The high-dose fluoxetine group showed decreased testosterone, increased LH and FSH, reduced seminiferous tubule sperm density, as well as fewer spermatogonia and primary spermatocytes versus controls. Histology revealed reduced germinal epithelium layers and increased vacuolization in the fluoxetine-treated mice. These findings demonstrate that chronic high-dose fluoxetine administration inhibits steroidogenesis and spermatogenesis in male mice, likely by increasing serotonin levels which suppress testosterone synthesis. Further research on fluoxetine's effects on male fertility are warranted given its widespread clinical use. This study affirms the need for judicious fluoxetine prescribing in patients with reproductive concerns.
