Dihydrotestosterone and the concept of 5α-reductase inhibition in human benign prostatic hyperplasia

  title={Dihydrotestosterone and the concept of 5$\alpha$-reductase inhibition in human benign prostatic hyperplasia},
  author={Georg Bartsch and Roger S. Rittmaster and Helmut Klocker},
  journal={World Journal of Urology},
Abstract. The development of human benign prostatic hyperplasia (BPH) clearly requires a combination of testicular androgens and the ageing process. Although the role of androgens as the causative factor for human benign prostatic hyperplasia is debated, they undoubtedly play, at least, a permissive role. The principal prostatic androgen is dihydrotestosterone. Although not elevated in human benign prostatic hyperplasia, dihydrotestosterone levels in the prostate remain at a normal level with… 
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  • Medicine, Biology
    Proceedings of the National Academy of Sciences
  • 2015
It is demonstrated that Anoctamin1 (ANO1) encodes a Ca2+-activated chloride channel that mediates various physiological functions and is essential for testosterone-induced BPH.
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    Expert opinion on investigational drugs
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Hormone modulators, which regulate the overgrowth of the prostate, represent one of the important categories that have been explored and that is still undergoing certain investigations towards the development of a therapeutic entity for the treatment of BPH.
Serotonin regulates prostate growth through androgen receptor modulation
Evidence is presented that links 5-HT depletion to BPH etiology through modulation of AR and that Serotoninergic prostate pathway should be explored as a new therapeutic target for BPH.
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In clinical practice, inhibitors of 5α-reductase (which converts testosterone to the more potent androgen dihydrotestosterone) have proven effective in the management of BPH, confirming an essential role for androgens in BPH pathophysiology.
Pao Pereira Extract Attenuates Testosterone-Induced Benign Prostatic Hyperplasia in Rats by inhibiting 5α-Reductase
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5α- Reductase Inhibitors in Prostate Cancer: An Overview
A brief account of biology of prostate, rationale and efficacy of 5AR inhibitors in prostate cancer management and their associated controversies is given.


Finasteride, an inhibitor of 5 alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia.
It is concluded that finasteride causes profound decrease in prostatic dihydrotestosterone levels in the prostates of men with benign prostatic hyperplasia.
Benign Prostatic Hyperplasia: Pathogenesis and Medical Therapy
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    Journal of the American Geriatrics Society
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Epidemiologic studies in castrates strongly support the key role of the testis in the pathogenesis of benign prostatic hyperplasia (BPH). Since the testis secretes androgen and estrogen, both of
The effect of finasteride in men with benign prostatic hyperplasia.
  • P. Walsh
  • Medicine
    The Journal of urology
  • 1993
The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction.
Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated rat.
Whereas DHT is more potent than testosterone at stimulating prostate epithelial cell function as measured by ductal mass, the two androgens are equipotent at preventing prostate cell death after castration, which explains why finasteride causes prostate involution in the rat with minimal evidence of prostate cellDeath.
Deletion of steroid 5α-reductase 2 gene in male pseudohermaphroditism
The results verify the existence of at least two 5α-reductases in man and provide insight into a fundamental hormone-mediated event in male sexual differentiation.
Testosterone at high concentrations interacts with the human androgen receptor similarly to dihydrotestosterone.
The results suggest that the weaker androgenic potency of testosterone compared to that of dihydrotestosterone resides in its weaker interaction with the androgen receptor, most clearly demonstrable as an increase in the dissociation rate of testosterone from the receptor.
Expression and regulation of steroid 5 alpha-reductase 2 in prostate disease.
Investigation of the expression of the type 2 isozyme of 5 alpha-reductase in benign prostatic hyperplasia and prostate cancer shows that androgen ablation therapies substantially decrease isozyme expression in the epididymis but have a lesser effect in the prostate.
Deletion of steroid 5 alpha-reductase 2 gene in male pseudohermaphroditism.
The results verify the existence of at least two 5 alpha-reductases in man and provide insight into a fundamental hormone-mediated event in male sexual differentiation.