Steroid sulfatase activity in epidermis of acne-prone and non-acne-prone skin of patients with acne vulgaris

Cutaneous Androgen Metabolism: Basic Research and Clinical Perspectives

“…Strong steroid sulfatase immunoreactivity in the acne skin, primarily associated with the monocytes in¢ltrating the lesions, but not in una¡ected skin was observed. The enzymatic hydrolysis of DHEA-S to DHEA and of estrone sulfate to estrone in cultured epidermal keratinocytes has been demonstrated (Milewich et al, 1990). There were no di¡erences in the rates of enzymatic hydrolysis of steroid sulfatase in the epidermis of acne-prone and nonacne-prone skin; however, the rate of estrone sulfate hydrolysis was two to eight times greater than that of DHEA-S in all of the tissues evaluated.…”

Androgens and androgen receptor action in skin and hair follicles

“…Although the skin can synthesize steroids de novo from cutaneous endogenous cholesterol, the main precursor used to produce steroids is adrenal DHEA-S. DHEA-S is hydrolyzed to DHEA by the steroid sulfatase located in sebaceous glands and dermal papilla cells (DPC) in terminal hair follicles [37,38] whereas enzymatic activity of 3β-HSD1 converts DHEA into androstenedione, and 17β-HSD3 converts androstenedione in testosterone [39]. 17β-HSD is present in 5 different isoforms that function as a switch on/off mechanism for the production of the most potent sexual steroids.…”

Steroidogenesis in the skin: Implications for local immune functions

“…In support of the latter, T synthesis by SZ95 sebocytes in vitro derives mainly from DHEA [93]. DHEA-S is hydrolysed in the skin to DHEA by steroid sulfatase, detected in sebaceous glands and dermal papilla cells (DPCs) of terminal HFs [94, 95]. Monocytes also exhibit steroid sulfatase activity, thus introducing the variable of “inflammation” to cutaneous androgen production [96].…”