Figure 2. Antiandrogenic Activity of Lavender and Tea Tree Oils in Breast-Cancer (MDA-kb2) Cells.
MDA-kb2 cells that were stably transfected with the MMTV-luciferase (firefly) plasmid were treated for 24 hours with increasing concentrations of lavender oil (Panel A) or tea tree oil (Panel B) in the presence or absence of DHT. The firefly luciferase activity was normalized to the total protein content for each sample. The data were averaged and plotted as the average (±SE) fold increase above vehicle control of three independent experiments performed in quadruplicate. The upper dashed lines in Panels A and B represent treatment of the cells with DHT alone, and the lower dashed lines represent treatment with DHT in the presence of flutamide. For the comparison between treatment with DHT and treatment with ethanol (the solvent control) alone, P<0.001. For the comparison between treatment with either DHT plus flutamide or DHT plus either lavender oil (at 0.001% and 0.005%) or tea tree oil (at 0.005%) and treatment with DHT alone, P<0.001. For the comparison between treatment with DHT plus tea tree oil at 0.0005% and treatment with DHT alone, P<0.05. For the comparison between treatment with tea tree oil at 0.001% and treatment with DHT alone, P<0.01. In Panel C, MDA-kb2 cells were treated with 0.1 nM DHT for 24 hours in the presence or absence of 0.005% (vol/vol) lavender oil, 0.005% (vol/vol) tea tree oil, or 1 µM of flutamide. Real-time PCR was performed to measure the steady-state mRNA concentrations of CYP4F8, C1orf116, UGT2B28, and SEC14L2. All values were normalized to β2-microglobulin, and each data point represents the average increase above vehicle control of the values obtained from three independent experiments performed in duplicate.
If you look at the chart…the oils could inhibit the androgen receptor (they didn’t affect the expression of the receptor, so they must be blocking it) every bit as well as flutamide. A smaller volume of flutamide was used, but the values below the activity in the pure DHT culture were profound. Obviously something in these oils blocks the androgen receptor.
I wonder if topical application in an adult male will yield unacceptable side effects?
If you look at the lavender chart…you will see that when .01 nM of lavender was cultivated with DHT, the inhibition of DHT was equal to that of on pM of pure flutamide, indicating that lavender can (at a higher concentraion, but still very little of it as a substance) inhibit the androgen receptor equal to flutamide. It took MORE of tea tree to get the inhibition of the androgen receptor down to flutamide levels (and indeed it never got all the way down to flutamide levels, but it got fairly close).
I wonder if topical lavender (again) would have bad side effects though…