Abstract
Both testosterone and 5α-dihydrotestosterone (DHT) increased the growth rate of androgendependent mouse mammary tumour cells (S115) in culture. DHT was effective at lower concentrations and increased the thymidine labelling index with a shorter lag-period than testosterone. The S115 cells converted testosterone to DHT, 5α-androstane-3α-17β-diol, androsterone and androstanedione. DHT was not converted to testosterone. All this data was consistent with the view that testosterone exerted its biological effect in this system by conversion to DHT. However, the high affinity, 8–9 cytoplasmic receptor bound testosterone as well as DHT. Testosterone competed with DHT for binding sites and vice versa; oestradiol 17β blocked the binding of both androgens but no binding of 3H-oestradiol-17β to an 8–9 component was detected. After incubation of cells with 3H-testosterone at 37 °C a 5S receptor could be extracted from nuclei. The major radioactive steroid in the nucleus under these conditions was testosterone. This binding data suggests that testosterone might be biologically active without metabolic conversion to DHT.
Published Version
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