Journal List > Korean J Androl > v.30(1) > 1033102

Park, Cho, and Paick: 5α-Reductase

Abstract

Androgen acts via the androgen receptor and can play a critical role in the development and growth of the prostate and the pathophysiology of prostatic diseases. Testosterone is the most abundant circulating androgen and is converted to dihydrotestosterone (DHT), a more potent androgen, by steroid 5α-reductase. There are two 5α-reductase isoenzymes, type 1 and type 2, in humans and animals. Type 2 5α-reductase predominates in the prostate. While deficiency of type 2 5α-reductase causes male pseudohermaphroditism, increased DHT has been implicated in benign prostatic hyperplasia and prostate cancer. The aim of this article is to highlight the significance of 5α-reductase in the development and growth of the prostate and pathogenesis of prostatic diseases.

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Table 1.
Comparison of the two human 5α-reductase isoenzymes
  Type 1 5α-reductase Type 2 5α-reductase
Gene structure 5 exons, 4 introns 5 exons, 4 introns
Gene chromosome location SRD5A1, 5p15 SRD5A2, 2p23
Size 259 amino acids 254 amino acids
Molecular weight (kilodaltons) 29,462 (or 29,000) 28,398 (or 28,000)
Homology 49% 49%
pH optima Neutral to basic (6∼8.5) Acidic to neutral (5.0∼5.5)
Testosterone affinity Km=1∼5 (or 1.5) μM Km=0.004∼1 (or 0.1∼1.0) μM
Half life 20∼30 hours 20∼30 hours
Tissue distribution Livers, sebaceous gland, nongenital Prostate, genital skin, seminal vesicles,
  skin, prostate, scalp, brain epididymis, liver, hair follicles, uterus, breasts, brain, placenta
Prostate level Low High
Prostate cell    
 Epithelial
 Basal
 Stromal
Prostate    
 Normal
 BPH
 Prostate cancer
Activity in 5αR deficiency Normal Mutated
Inhibitor Dutasteride Finasteride, dutasteride
Finasteride inhibition Ki≥300 nM Ki≥3∼5 nM

5p15: chromosome 5 band 15, 2p23: chromosome 2 band 23, BPH: benign prostatic hyperplasia, 5αR: 5αreductase.

The Km of 5α-reductase-2 for testosterone is dependent on the assay condition.

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