Prolactin effect on the permeability of human benign hyperplastic prostate to testosterone

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Abstract
While it has been known for over 30 years that prolactin (Prl) synergizes with androgen in the support and stimulation of prostatic growth and metabolism, the evidence that this is accomplished through increasing access of the steroid to the cellular machinery of the gland has arisen only since about 1970. There is widespread uncertainty as to how the Prl effect takes place: by 1) increasing the free steroid concentration in the blood; 2) facilitating the uptake of protein‐bound androgen; 3) increasing, by metabolism or receptor‐binding, the concentration gradient that can support passive diffusion of the steroid across the plasma membrane; or 4) modification of the fluidity of the membrane itself to increase the solubility of the steroid in the lipoprotein and, thus, the ease of penetration of the cell. The present study attempted to learn if Prl is an effective stimulus of androgen uptake when the first three options are not operative. Using an equilibrium exchange procedure to track the uptake of [17α‐3H]‐testosterone ([17α‐3H]‐T) into minced benign hyperplastic human prostate tissue and the irreversible metabolism of the entering steroid to [17α‐3H]‐dihydrotestosterone [17α‐3H]‐DHT, it was found that the rate of production of the 5α‐reduced metabolite, during a 1‐hr incubation in vitro, was directly proportional to the concentration of ovine Prl over the dose range of 0–160 ng/ml. The clinical significance of Prl mediation of steroid uptake is discussed, and suggestions are made as to how the Prl might alter the permeability of the plasma membrane.