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Testosterone boosts fluid and electrolyte secretion in seminal vesicles, aiding sperm function.

Testosterone makes the connections in the uterus lining simpler and lowers certain protein levels, which might lead to infertility.

A new genetic change causing early stop in the androgen receptor gene was found in a patient with androgen insensitivity syndrome.

Two new mutations in the AR gene linked to severe androgen insensitivity were found.

The ABI1 gene contributes to prostate cancer progression and treatment resistance.

Dihydrotestosterone treatment can help penis growth in boys with 5α-reductase deficiency but doesn't fully normalize size after puberty.

Testosterone can build muscle and bone without enlarging the prostate when a specific enzyme is blocked.

SHISA6 helps maintain certain stem cells in mouse testes by blocking signals that would otherwise cause them to differentiate.

Resveratrol helps prevent finasteride-induced damage in male rats, improving reproductive function.

GnRH treatment can reduce breast cancer cell invasion.

Some antiandrogens may lower testosterone better than others, but it's unclear which is best for feminization in transgender women; more research is needed.

Plant-based compounds might be effective, low-side-effect treatments for prostate cancer by blocking a specific enzyme.

SRD5A1 is crucial in advanced prostate cancer, and blocking both SRD5A1 and SRD5A2 is more effective than targeting SRD5A2 alone.

A genetic defect causes males in some Mediterranean populations to be born with ambiguous genitalia and develop male traits at puberty.

Certain compounds reduced hamster flank organ size by inhibiting 5α-reductase, like finasteride, without affecting androgen receptors.

SHH protein helps nerve regeneration in hypertensive rats.

Deleting the CDSN gene causes severe skin and hair problems, leading to death.

Genetic differences within ethnic groups may affect prostate cancer treatment effectiveness.

Masculinization in affected individuals occurs gradually after puberty due to hormone changes.

DHT deficiency may disrupt rat epididymis function by affecting estrogen receptors.

5-alpha-reductase inhibitors significantly affect the penile tissue of hypertensive rats.

Androgens regulate Sertoli cells and affect fertility through specific receptors and coregulators.

Finasteride exposure in pregnancy causes genital abnormalities in male rats.

The equine epididymis mainly uses type 1 5α-reductase, and both finasteride and dutasteride can inhibit its activity.

5-α-reductase inhibitors reduce prostate cancer risk but may cause sexual dysfunction and don't affect high-grade tumor or death rates.

5α-reductase inhibitors like finasteride may not be effective or safe for transgender individuals, and more research is needed.

Long-term use of certain prostate drugs can worsen erectile dysfunction by changing penile tissue, especially in rats with high blood pressure.

Prostate cancer patients need early psychological and sexual support during radiotherapy to improve their quality of life.

Higher SRD5A2 expression predicts better response to finasteride in treating urinary symptoms.