DOSE-DEPENDENT EFFECTS OF TAMSULOSIN ON TESTICULAR HISTOLOGY AND REPRODUCTIVE FUNCTION

Main Article Content

Sofia Jadoon
Yasir Humayun
Nighat Parveen
Saadia Sadiq
Anila Farid

Keywords

Tamsulosin, Testicular histology, Johnsen score, Leydig cells, Spermatogenesis

Abstract

Introduction: Tamsulosin, an α1A-adrenoceptor antagonist commonly used for lower urinary tract symptoms, may affect male reproductive function by altering testicular microarchitecture. Understanding its dose-dependent impact on seminiferous tubules and interstitial cells is essential for evaluating reproductive safety.


Objective: To investigate the dose-dependent effects of tamsulosin on testicular histology and function, focusing on structural changes within seminiferous tubules and interstitial compartments.


Methodology: Thirty adult albino mice were divided into three groups: control, low-dose (8 µg/kg/day), and high-dose (16 µg/kg/day) tamsulosin, administered for 45 days. Testes were collected, fixed, processed, and stained with hematoxylin and eosin for histopathological evaluation. Seminiferous tubule integrity, germ cell maturation, Leydig cell count, and tunica albuginea thickness were assessed using standardized Johnsen scoring. Data were analyzed with ANOVA and Tukey post hoc tests.


Results: Control testes showed preserved seminiferous architecture with complete spermatogenesis. Low-dose tamsulosin induced mild disorganization of germinal epithelium, while high-dose exposure caused marked degeneration of seminiferous tubules, spermatogenic arrest, and altered interstitial Leydig cell populations. Johnsen scores were significantly reduced in the high-dose group (p ≤ 0.05), whereas tunica albuginea thickness remained unchanged.


Conclusion: Tamsulosin induces dose-dependent testicular histopathological alterations, with higher doses producing significant seminiferous tubular degeneration and interstitial cell changes. These findings highlight the importance of histological evaluation in assessing the reproductive safety of α1A-adrenoceptor antagonists.


 


 

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