Assessment of the androgenic potencies of phytoestrogens with and without co-incubated testosterone by using TARM-Luc cell line

The ability of the prostate gland to grow is a hormone-dependent process that is regulated by both androgenic and estrogenic factors. Phytoestrogens (PEs) are bioactive compounds with the estrogenic activity which may impact hormones and health in general. The TARM-Luc cell line was used in this study to investigate the androgenic potencies of phytoestrogens with and without co-incubated testosterone. The transcriptional activities (TAs) of 10 PEs (apigenin, daidzein, daidzin, equol, enterodiol, formononetin, genistein, genistin, glycitein, and matairesinol) were assessed as induction of the expressed luciferase activity, which is connected with the biological effects. These effects were compared to transcription caused by testosterone (50 nM) hormone (standards) in vitro. Androgenic receptors in the TARM-Luc cell line were used in the reporter gene assay tool. The standard curve for hormone standard was determined and the EC50 (M) for testosterone was (3.7 x 10-9 M). The order of androgenic potency of two PEs from their EC50s was apigenin (4.5 X 10-6 M) > glycitein (4.8 X 10-5 M). Dose-response curves in the TARM-Luc cell line, for the other eight PEs, were not established as most were anti-androgenic. The percent androgenic potency for apigenin was 8.2 x 10-2 M and for glycitein was 7.7 x 10-3 M relative to testosterone whose percent potency was arbitrarily assigned a value of 100. PEs inhibition or enhancement on the hormone testosterone (50 nM) -dependent transcription was dose-dependent and chemically specific. PEs enhanced testosterone hormone-dependent transcription and gave more additive and synergistic bioactive effects in a dose-dependent manner. Two PEs, apigenin and glycitein, were weak agonists in TARM-Luc cell line. The additive and synergistic effects of the PEs in combination with testosterone (50 nM) were a novel discovery in this study and relevant since it could have endocrine disrupting effects.