Neural injections of Bromodeoxyuridine (BrdU) were applied to males of both groups to test for neurogenesis . Analysis showed that testosterone and dihydrotestosterone regulated adult hippocampal neurogenesis (AHN). Adult hippocampal neurogenesis was regulated through the androgen receptor in the wild-type male rats, but not in the TMF male rats. To further test the role of activated androgen receptors on AHN, flutamide , an antiandrogen drug that competes with testosterone and dihydrotestosterone for androgen receptors , and dihydrotestosterone were administered to normal male rats. Dihydrotestosterone increased the number of BrdU cells, while flutamide inhibited these cells.
Looking at the list below can tell you whether or not something may increase your risk of cancer, but it is important to try to get an idea of how much it might increase your risk. It is also important to know what your risk is to begin with. Many factors can enter into this, including your age, gender, family history, and lifestyle factors (tobacco and alcohol use, weight, diet, physical activity level, etc.). As noted above, the type and extent of exposure to a substance may also play a role. You should consider the actual amount of increased risk when deciding if you should limit or avoid an exposure.
Aromatase inhibitors are the compounds that serve to reduce estradiol levels in blood by eliminating the production of estradiol through binding to and disabling the aromatase enzyme, which is responsible for the conversion (or aromatization) of androgens into estradiol. Suicidal aromatase inhibitors serve to permanently inhibit and disable the aromatase enzyme to which it is bound to. This renders the enzyme inactive forever. The body will eventually manufacture more aromatase enzymes, but the currently-bound enzymes are bound indefinitely, eliminating any risk for estrogen rebound. This is the main difference compared alongside two other major aromatase inhibitors: anastrozole and letrozole, which are non-suicidal aromatase inhibitors that are only bound to the aromatase enzyme for limited time periods. If a non-suicidal aromatase inhibitor is halted too abruptly, the circulating inhibited aromatase enzymes that have not been metabolized out of the body will then become free again, and begin aromatizing androgens into estrogens at an often rapid rate. This is not the case with Exos.