Journal
HORMONE AND METABOLIC RESEARCH
Volume 39, Issue 2, Pages 141-148Publisher
GEORG THIEME VERLAG KG
DOI: 10.1055/s-2007-961814
Keywords
androgens; anti-androgens; 5 alpha-reductase inhibitors; sebaceous gland; keratinocytes; cell proliferation; acne
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Inhibition of 5 alpha-reductase type 1 has been considered to be a promising target for treatment of androgen-dependent skin disorders, however, currently published clinical results on acne treatment are rather disappointing. in this study, the influence of selective inhibitors of 5 alpha-reductase on testosterone metabolism within SZ95 sebocytes and HaCaT keratinocytes in vitro was investigated. In both cell types, the iscitype 1 inhibitor MK386 completely inhibited the conversion of testosterone to 5 alpha-dihydrotestosterone in concentrations higher than 10(-9)M. Inhibitors of the isotype 2 such as finasteride, clihydrofinasteride, and turosteride, were > 100-fold less active, while, as expected, androgen receptor inhibitors did not affect the 5a-reductase activity. MK386, but not finasteride, reduced testosterone-stimulated Proliferation and slightly reduced the testosterone-induced increase in the amount of SZ95 sebocyte proteins. The androgen receptor inhibitor cyproterone acetate exhibited no effect on testosterone-induced proliferation, but inhibited the 5 alpha-dihydrotestosterone-induced sebocyte proliferation. Our experimental findings and the existing clinical results indicate that the inhibition of 5a-reductase activity alone may be insufficient to reduce overall sebocyte activity and improve acne lesions.
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