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1. C. In adolescent males, testicular testosterone production dramatically rises from prepuberal levels and then declines into adulthood. However, with advancing adulthood there is a drop in the metabolic clearance rate of testosterone, increasing the length of time that testosterone remains in the serum. Evidence of a relatively constant level of serum testosterone is seen in the relative constant levels of urinary 17-ketosteroids, a metabolite of testosterone, from the second to the fifth decade of life.

2. D. The enzyme 5a-reductase catalyzes the formation of dihydrotestosterone from testosterone. In normal accessory sex gland tissues, such as the prostate, most of the direct androgen effect is due to dihydrotestosterone rather than testosterone. Thus when 5a-reductase is lacking, serum levels of testosterone may be normal or even slightly elevated with a hypotrophied prostate gland.

3. A. In the Leydig cell the rate-limiting step in testosterone synthesis is the enzymatic cleavage of side chains from cholesterol to form pregnenolone.

4. D. Skeletal muscle cells use the androgen receptor to bind testosterone that promotes the anabolic effect of this hormone.

5. B. Finasteride is a 5a-reductase inhibitor, which essentially makes dihydrotestosterone unavailable to the prostate but does not reduce serum testosterone levels. The decreased prostatic levels of dihy-drotestosterone frequently result in a size regression of the prostate, while the relatively normal testosterone levels minimize a depressed libido. Flutamide and spironolactone exhibit antiandrogen effects by competing for the androgen receptor; ketoconazole inhibits testosterone synthesis; and stanozolol is an oral anabolic androgen preparation.

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