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Updated: May 13, 2026

Murine Orchiectomy and Ovariectomy to Reduce Sex Hormone Production
Published on: November 17, 2023
Effects of supraphysiological testosterone treatment and orchiectomy on ischemia/reperfusion-induced bladder
Shu-Mien Chuang1, Keh-Min Liu, Yung-Chin Lee
1Yuh-Ing Junior College of Health Care and Management, Kaohsiung, Taiwan.
Introduction:
The roles of testosterone and orchiectomy on male bladder subjected to ischemic/reperfusion (I/R) injuries received little attention. To fill this gap, the present study intended to examine testosterone and orchiectomy effects on male rabbits subjected to I/R damages.
Aim:
To elucidate the effects of testosterone and orchiectomy on contractile response, bladder morphology, interstitial fibrosis, and oxidative stress in male rabbit bladder subjected to I/R surgery.
Methods:
Male New Zealand rabbits were distributed into five groups as follows: Group 1 received sham surgical procedure. In group 2, I/R surgery was performed. In group 3, testosterone (100 μg/kg/day) was intramuscularly injected prior to I/R surgery. In group 4, orchiectomy was performed prior to I/R surgery. In group 5, orchiectomy was performed with subsequent testosterone administration, followed by I/R surgery. All the rabbits were euthanized 7 days after I/R. Comparative studies were analyzed to elucidate the effects of testosterone and orchiectomy on bladder dysfunction subjected to I/R injuries.
Main Outcome Measures:
Bladder contractile function was evaluated. Masson's trichrome staining and immunohistochemical studies were performed to evaluate bladder morphology and intramural nerve terminals. Western blotting was examined to investigate the expressions of fibrosis and oxidative stress markers.
Results:
I/R surgery significantly decreased bladder contractility in response to various stimulations with and without testosterone treatment. I/R damages decreased bladder nerve density with and without testosterone. The expressions of fibrosis and oxidative stress-related proteins were increased by I/R injuries with or without testosterone treatment. Testosterone depletion significantly decreased the expressions of transforming growth factor-β and fibronectin expressions after I/R injury. Supraphysiological testosterone treatment after orchiectomy greatly increased the expressions of these fibrosis proteins; however, orchiectomy alone ameliorated I/R injuries.
Conclusions:
Testosterone treatment or orchiectomy affected I/R-induced bladder damages in male rabbits. Orchiectomy decreased the level of fibrosis and oxidative stress markers and increased neurofilament densities. Supraphysiological exogenous testosterone administration after orchiectomy further exacerbated such detrimental effects of I/R.
Insights
Orchiectomy ameliorated ischemic/reperfusion (I/R) bladder injury in male rabbits by reducing fibrosis and oxidative stress. However, testosterone administration exacerbated these I/R-induced damages.
Area of Science:
- Urology
- Andrology
- Pathology
Background:
- Ischemic/reperfusion (I/R) injury impacts male bladders, with limited understanding of hormonal influences.
- Testosterone and orchiectomy roles in I/R-induced bladder damage require investigation.
Purpose of the Study:
- To investigate the effects of testosterone and orchiectomy on male rabbit bladders subjected to I/R injury.
- To assess changes in bladder contractility, morphology, fibrosis, and oxidative stress.
Main Methods:
- Male New Zealand rabbits underwent sham surgery, I/R, I/R with testosterone, orchiectomy followed by I/R, or orchiectomy with testosterone then I/R.
- Bladder contractility, morphology, nerve density, fibrosis, and oxidative stress markers were evaluated.
Main Results:
- I/R injury reduced bladder contractility and nerve density, while increasing fibrosis and oxidative stress markers.
- Orchiectomy alone improved I/R outcomes, decreasing fibrosis and oxidative stress.
- Testosterone administration, especially supraphysiological doses post-orchiectomy, worsened I/R damage.
Conclusions:
- Orchiectomy mitigates I/R-induced bladder damage by reducing fibrosis and oxidative stress and preserving nerve density.
- Exogenous testosterone exacerbates I/R injury, highlighting its complex role in bladder pathophysiology.
