SRD5A2 Gene

Meaning

The SRD5A2 gene provides instructions for creating the steroid 5-alpha reductase type 2 enzyme. This enzyme converts testosterone, a less potent androgen, into dihydrotestosterone, a significantly more potent androgen. Its activity is fundamental to androgenic signaling.

Context

This gene functions prominently within androgen-responsive tissues, including the prostate gland, seminal vesicles, epididymis, and external genitalia, particularly during fetal development and puberty. It also contributes to androgen action in adult hair follicles and sebaceous glands. Localized activity ensures tissue-specific androgenic effects.

Significance

Clinically, variations within the SRD5A2 gene are crucial for understanding conditions related to androgen action. Mutations in this gene can lead to 5-alpha reductase deficiency, a disorder of sex development characterized by impaired virilization in XY individuals. Common genetic variations, or polymorphisms, within SRD5A2 are associated with susceptibility to benign prostatic hyperplasia, prostate cancer, and androgenetic alopecia.

Mechanism

The SRD5A2 gene encodes the 5-alpha reductase type 2 enzyme, which catalyzes the irreversible reduction of testosterone’s delta-4,5 double bond at the A-ring to form dihydrotestosterone. This enzymatic conversion occurs intracellularly and is a critical step in amplifying androgenic signals in target cells. The enzyme utilizes NADPH as a cofactor.

Application

Genetic analysis of the SRD5A2 gene is routinely employed in the diagnostic workup for individuals presenting with atypical genitalia or suspected disorders of sex development. Pharmacological agents, specifically 5-alpha reductase inhibitors like finasteride and dutasteride, are clinically applied to reduce DHT levels, thereby managing benign prostatic hyperplasia and androgenetic alopecia. These medications target this gene’s encoded enzyme.

Metric

Assessment of SRD5A2 enzyme activity or gene function often involves measuring serum testosterone to dihydrotestosterone (T/DHT) ratios, which are typically elevated in cases of 5-alpha reductase deficiency. Molecular genetic testing, including sequencing of the SRD5A2 gene, confirms specific mutations. Clinical evaluation of secondary sexual characteristics and response to androgen administration provides diagnostic insight.

Risk

Dysregulation of SRD5A2 activity or therapeutic inhibition carries specific clinical considerations. Congenital 5-alpha reductase deficiency, if not recognized, can challenge gender identity and psychosocial well-being. Pharmacological inhibition of the enzyme can lead to adverse effects such as sexual dysfunction, including decreased libido and erectile dysfunction, gynecomastia, and potential mood changes in some individuals. Clinical monitoring is essential.

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