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Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells.
Urology. 1996 Oct; 48(4):654-9.U

Abstract

OBJECTIVES

The function of the prostate gland in many animals, including humans, is to accumulate and secrete large quantities of citrate. This function derives from the metabolic characteristics of the prostate secretory epithelial cells. These cells possess a uniquely limiting mitochondrial aconitase (m-aconitase) that minimizes citrate oxidation and thus permits citrate to accumulate. Unfortunately, the characteristics of prostate m-aconitase and its manner of regulation have not been established. The hormones testosterone and prolactin, however, are significantly involved in regulating prostate citrate production. Thus 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 level of m-aconitase enzyme, on the level of m-aconitase activity, and on citrate utilization. The epithelial cells were incubated for 3 hours with either testosterone (10(-9) M), prolactin (1 microgram/mL), or vehicle (control).

RESULTS

Both hormone applications caused a marked increase in the level of m-aconitase. In contrast, neither hormone had any effect on the m-aconitase level of pig seminal vesicle cells, which are also citrate-producing cells. Moreover, neither hormone had any effect on pyruvate dehydrogenase E1a. These findings suggest that testosterone and prolactin regulation of prostate m-aconitase is a highly specific effect. Along with the increase in the level of m-aconitase enzyme, both hormones also increased m-aconitase activity and prostate-cell utilization of citrate.

CONCLUSIONS

These studies demonstrate that testosterone and prolactin can regulate m-aconitase and sub-sequent citrate oxidation of specific prostate epithelial cells. This unique aconitase relationship is not observed in other mammalian cells.

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Authors+Show Affiliations

Costello LC
Dental School, University of Maryland, Baltimore, USA.
Liu Y
No affiliation info available
Franklin RB
No affiliation info available

MeSH

Aconitate HydrataseAnimalsCells, CulturedCitric Acid CycleEpithelial CellsEpitheliumMaleMitochondriaProlactinProstateSwineTestosterone

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8886079

Citation

Costello, L C., et al. "Testosterone and Prolactin Stimulation of Mitochondrial Aconitase in Pig Prostate Epithelial Cells." Urology, vol. 48, no. 4, 1996, pp. 654-9.
Costello LC, Liu Y, Franklin RB. Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells. Urology. 1996;48(4):654-9.
Costello, L. C., Liu, Y., & Franklin, R. B. (1996). Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells. Urology, 48(4), 654-9.
Costello LC, Liu Y, Franklin RB. Testosterone and Prolactin Stimulation of Mitochondrial Aconitase in Pig Prostate Epithelial Cells. Urology. 1996;48(4):654-9. PubMed PMID: 8886079.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Testosterone and prolactin stimulation of mitochondrial aconitase in pig prostate epithelial cells. AU - Costello,L C, AU - Liu,Y, AU - Franklin,R B, PY - 1996/10/1/pubmed PY - 1996/10/1/medline PY - 1996/10/1/entrez SP - 654 EP - 9 JF - Urology JO - Urology VL - 48 IS - 4 N2 - OBJECTIVES: The function of the prostate gland in many animals, including humans, is to accumulate and secrete large quantities of citrate. This function derives from the metabolic characteristics of the prostate secretory epithelial cells. These cells possess a uniquely limiting mitochondrial aconitase (m-aconitase) that minimizes citrate oxidation and thus permits citrate to accumulate. Unfortunately, the characteristics of prostate m-aconitase and its manner of regulation have not been established. The hormones testosterone and prolactin, however, are significantly involved in regulating prostate citrate production. Thus 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 level of m-aconitase enzyme, on the level of m-aconitase activity, and on citrate utilization. The epithelial cells were incubated for 3 hours with either testosterone (10(-9) M), prolactin (1 microgram/mL), or vehicle (control). RESULTS: Both hormone applications caused a marked increase in the level of m-aconitase. In contrast, neither hormone had any effect on the m-aconitase level of pig seminal vesicle cells, which are also citrate-producing cells. Moreover, neither hormone had any effect on pyruvate dehydrogenase E1a. These findings suggest that testosterone and prolactin regulation of prostate m-aconitase is a highly specific effect. Along with the increase in the level of m-aconitase enzyme, both hormones also increased m-aconitase activity and prostate-cell utilization of citrate. CONCLUSIONS: These studies demonstrate that testosterone and prolactin can regulate m-aconitase and sub-sequent citrate oxidation of specific prostate epithelial cells. This unique aconitase relationship is not observed in other mammalian cells. SN - 0090-4295 UR - https://www.unboundmedicine.com/medline/citation/8886079/Testosterone_and_prolactin_stimulation_of_mitochondrial_aconitase_in_pig_prostate_epithelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0090-4295(96)00217-8 DB - PRIME DP - Unbound Medicine ER -