TESTOSTERONE AND PROLACTIN STIMULATION OF MITOCHONDRIAL ACONITASE IN PIG PROSTATE EPITHELIAL-CELLS

Objectives. The function of the prostate gland in many animals, includ ing humans, is to accumulate and secrete large quantities of citrate. This function derives from the metabolic characteristics of the prosta te secretory epithelial cells. These cells possess a uniquely limiting mitochondrial aconitase (m-aconitase) that minimizes citrate oxidatio n and thus permits citrate to accumulate. Unfortunately, the character istics of prostate m-aconitase and its manner of regulation have not b een established. The hormones testosterone and prolactin, however, are significantly involved in regulating prostate citrate production. Thu s it is reasonable to hypothesize that these hormones may be involved in the regulation of both m-aconitase and citrate oxidation. Methods. Using freshly prepared pig prostate epithelial cells, we attempted to determine the effects of testosterone and prolactin treatment on the l evel of m-aconitase enzyme, on the level of m-aconitase activity, and on citrate utilization. The epithelial cells were incubated for 3 hour s with either testosterone (10(-9) M), prolactin (1 mu g/mL), or vehic le (control). Results. Both hormone applications caused a marked incre ase in the level of m-aconitase. In contrast, neither hormone had any effect on the m-aconitase level of pig seminal vesicle cells, which ar e also citrate-producing cells. Moreover, neither hormone had any effe ct on pyruvate dehydrogenase Ela. These findings suggest that testoste rone and prolactin regulation of prostate m-aconitase is a highly spec ific effect. Along with the increase in the level of m-aconitase enzym e, both hormones also increased m-aconitase activity and prostate-cell utilization of citrate. Conclusions. These studies demonstrate that t estosterone and prolactin can regulate m-aconitase and subsequent citr ate oxidation of specific prostate epithelial cells. This unique aconi tase relationship is not observed in other mammalian cells.