In this research, we plan on injecting three different groups of mice with varying amounts of testosterone propionate intraperitonially. One group will be given a low dose, one a moderate dose, and the last a high dose, while keeping one group as the control given no testosterone. Blood samples will be taken throughout the experiment to assess blood DHT levels in each of the groups. After the experiment is completed, we plan on taking a group weight of the prostate and determining whether there was a correlation between testosterone dose administration and DHT levels as well as a correlation between both hormone levels and prostate hyperplasia. The expected outcome of this experiment is that while increasing testosterone dosages and levels will lead to a logistic increase in DHT levels, there will be no effect on prostate hyperplasia. This hypothesis is based on Michaelis Menten kinetics and recent research on prostate hyperlasia. As levels of testosterone increase in the blood, there are only so many 5-alpha-reductase enzymes that can bind the free testosterone that eventually there will be a plateau in conversion to DHT. The rest of the free testosterone may remain free, be bound to aromatase enzyme and convert to estradiol, become bound to sex hormone binding globulin (SHBG), etc. Based on this enzyme kinetics and regulatory mechanisms, it is rational to hypothesize that testosterone and DHT may have direct logistic correlation, but do not result in prostate cell proliferation at higher levels.

Effect of exogenous testosterone administration on blood DHT levels and prostate hyperlasia in adult male mice

253rd National Meeting (2017)

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