The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Other undesirable androgenic consequences include aggressiveness, increase or decrease in libido, more pronounced hair growth on the face and body, changes in skin hue, oily skin and acne. The propionate ester may also worsen the condition of individuals already predisposed to male pattern baldness. A counteracting treatment regimen may be needed, but there are no guarantees to minimise hair loss. Testosterone products inhibit the body’s natural production of testosterone. To combat the crash, a drug to stimulate testosterone may be prescribed.