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A dose-dependent dual effect of oestrogen on voiding in the male mouse?
Tomi K Streng1, Antti Talo, Karl-Erik Andersson
1Department of Anatomy, Institute of Biomedicine, University of Turku, Turku, Finland.
Objectives:
To explore the effect of different degrees of oestrogenization on male voiding, by treating adult castrated and 5alpha-dihydrotestosterone (DHT)-maintained male mice with different doses of oestrogens, as exposure of male mice to excessive amounts of oestrogens can cause bladder outlet obstruction (BOO); in addition, male mice lacking oestrogen receptor (ER)alpha (ERKO) or ERbeta (BERKO) were studied to assess the importance of ER subtypes.
Materials And Methods:
Castrated, DHT-maintained adult mice were treated with 17beta-oestradiol (E(2); 50 and 250 microg/kg) or oestrone (E(1); 5, 50 and 500 microg/kg) daily for 10 days. Control mice were treated only with the vehicle. BERKO and ERKO mice, and their wild-type littermates used as their controls, remained untreated. Under anaesthesia, the bladder and distal urethra were exposed to record simultaneously the bladder pressure and urinary flow rate from the distal urethra.
Results:
E(2)-treated mice showed obstructive voiding, seen as increased bladder pressure, decreased average flow rate and prolonged micturition time. This was also evident when a high dose (500 microg/kg) of E(1) was used. After treatment with a dose of 50 microg/kg, the urodynamic variables were similar to those in the control mice. Surprisingly, after treatment with a low dose (5 microg/kg) all urodynamic variables improved. There was a minor increase in the bladder pressure in BERKO mice; ERKO mice had a significantly lower urinary flow rate.
Conclusions:
High doses of oestrogens caused BOO in castrated, DHT-maintained male mice. A small dose of E(1) had a positive effect on voiding, suggesting that oestrogens are needed for normal male voiding. Reduced urinary flow rates in ERKO mice suggest that oestrogen effects on voiding are mediated at least partly via ERalpha.
Insights
High estrogen doses cause bladder outlet obstruction in male mice, but low doses improve voiding. Estrogen receptor alpha plays a role in male urinary function.
Area of Science:
- Urology
- Endocrinology
- Reproductive Biology
Background:
- Estrogen's role in male physiology is complex and not fully understood.
- Oestrogenization can lead to bladder outlet obstruction (BOO) in male mice.
- Estrogen receptor (ER) subtypes, ERalpha and ERbeta, mediate estrogenic effects.
Purpose of the Study:
- To investigate the impact of varying estrogen levels on male voiding function.
- To determine the role of ERalpha and ERbeta in mediating estrogen's effects on male voiding.
- To assess the potential of estrogen therapy for improving male voiding dysfunction.
Main Methods:
- Adult castrated mice, maintained on 5alpha-dihydrotestosterone (DHT), were treated with different doses of 17beta-estradiol (E2) or estrone (E1).
- Urodynamic parameters including bladder pressure and urinary flow rate were measured.
- Male mice lacking ERalpha (ERKO) or ERbeta (BERKO) and their wild-type littermates were studied.
Main Results:
- High doses of E2 and E1 induced BOO, characterized by increased bladder pressure and decreased flow rate.
- A low dose of E1 (5 microg/kg) improved all urodynamic variables.
- ERKO mice exhibited significantly reduced urinary flow rates, while BERKO mice showed a minor increase in bladder pressure.
Conclusions:
- Excessive estrogen exposure can cause BOO in male mice.
- Low-dose estrogen, specifically E1, demonstrates a beneficial effect on male voiding.
- Estrogen's influence on male voiding is, at least partially, mediated through ERalpha.
