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Testosterone stimulates the biosynthesis of m-aconitase and citrate oxidation in prostate epithelial cells.
Mol Cell Endocrinol. 1995 Jul; 112(1):45-51.MC

Abstract

Mitochondria (m-)aconitase is a rate-limiting regulatory enzyme in prostate epithelial cells which minimizes citrate oxidation by these cells. This unique metabolite characteristic is responsible for the ability of the prostate to accumulate and secrete extraordinarily high levels of citrate. Testosterone is a major regulator of prostate growth and function, and stimulates citrate oxidation. Therefore, an important action of testosterone might be its stimulation of m-aconitase in prostate epithelial cells. Studies were conducted with rat ventral prostate (VP) epithelial cells to establish the effect of testosterone on the level of m-aconitase and corresponding citrate oxidation. Physiological concentrations (10(-7)-10(-10) M) of testosterone in vitro markedly increased the level of m-aconitase in freshly prepared isolated prostate epithelial cells. This increase was apparent within 3 h of exposure to the hormone. The stimulatory effect of testosterone on m-aconitase was abolished by actinomycin D and by cycloheximide. Both the level of m-aconitase enzyme and the level of m-aconitase activity were similarly increased by testosterone treatment. Correspondingly, testosterone increased the rate of mitochondrial citrate oxidation while having no effect on the rate of isocitrate oxidation, thereby demonstrating that the action of testosterone is specifically targeted at the m-aconitase reaction. In vivo studies revealed that castration markedly decreased and testosterone administration increased the m-aconitase level of prostate epithelial cells. In contrast, neither liver nor kidney m-aconitase level was altered by castration. These studies demonstrate that testosterone regulates the biosynthesis of m-aconitase in prostate epithelial cells.(

ABSTRACT

TRUNCATED AT 250 WORDS)

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Authors+Show Affiliations

Costello LC
Department of Physiology, University of Maryland Dental School, Baltimore 21201, USA.
Liu Y
No affiliation info available
Franklin RB
No affiliation info available

MeSH

Aconitate HydrataseAnimalsBlotting, WesternCitratesCitric AcidCycloheximideDactinomycinEpitheliumKineticsMaleMitochondriaOrchiectomyOxidation-ReductionProstateProtein Synthesis InhibitorsRatsSonicationTestosterone

Pub Type(s)

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

Language

eng

PubMed ID

7589784

Citation

Costello, L C., et al. "Testosterone Stimulates the Biosynthesis of M-aconitase and Citrate Oxidation in Prostate Epithelial Cells." Molecular and Cellular Endocrinology, vol. 112, no. 1, 1995, pp. 45-51.
Costello LC, Liu Y, Franklin RB. Testosterone stimulates the biosynthesis of m-aconitase and citrate oxidation in prostate epithelial cells. Mol Cell Endocrinol. 1995;112(1):45-51.
Costello, L. C., Liu, Y., & Franklin, R. B. (1995). Testosterone stimulates the biosynthesis of m-aconitase and citrate oxidation in prostate epithelial cells. Molecular and Cellular Endocrinology, 112(1), 45-51.
Costello LC, Liu Y, Franklin RB. Testosterone Stimulates the Biosynthesis of M-aconitase and Citrate Oxidation in Prostate Epithelial Cells. Mol Cell Endocrinol. 1995;112(1):45-51. PubMed PMID: 7589784.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Testosterone stimulates the biosynthesis of m-aconitase and citrate oxidation in prostate epithelial cells. AU - Costello,L C, AU - Liu,Y, AU - Franklin,R B, PY - 1995/7/1/pubmed PY - 1995/7/1/medline PY - 1995/7/1/entrez SP - 45 EP - 51 JF - Molecular and cellular endocrinology JO - Mol Cell Endocrinol VL - 112 IS - 1 N2 - Mitochondria (m-)aconitase is a rate-limiting regulatory enzyme in prostate epithelial cells which minimizes citrate oxidation by these cells. This unique metabolite characteristic is responsible for the ability of the prostate to accumulate and secrete extraordinarily high levels of citrate. Testosterone is a major regulator of prostate growth and function, and stimulates citrate oxidation. Therefore, an important action of testosterone might be its stimulation of m-aconitase in prostate epithelial cells. Studies were conducted with rat ventral prostate (VP) epithelial cells to establish the effect of testosterone on the level of m-aconitase and corresponding citrate oxidation. Physiological concentrations (10(-7)-10(-10) M) of testosterone in vitro markedly increased the level of m-aconitase in freshly prepared isolated prostate epithelial cells. This increase was apparent within 3 h of exposure to the hormone. The stimulatory effect of testosterone on m-aconitase was abolished by actinomycin D and by cycloheximide. Both the level of m-aconitase enzyme and the level of m-aconitase activity were similarly increased by testosterone treatment. Correspondingly, testosterone increased the rate of mitochondrial citrate oxidation while having no effect on the rate of isocitrate oxidation, thereby demonstrating that the action of testosterone is specifically targeted at the m-aconitase reaction. In vivo studies revealed that castration markedly decreased and testosterone administration increased the m-aconitase level of prostate epithelial cells. In contrast, neither liver nor kidney m-aconitase level was altered by castration. These studies demonstrate that testosterone regulates the biosynthesis of m-aconitase in prostate epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0303-7207 UR - https://www.unboundmedicine.com/medline/citation/7589784/Testosterone_stimulates_the_biosynthesis_of_m_aconitase_and_citrate_oxidation_in_prostate_epithelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/030372079503582R DB - PRIME DP - Unbound Medicine ER -