Journal
MITOCHONDRION
Volume 5, Issue 3, Pages 143-153Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2005.02.001
Keywords
prostate citrate metabolism; terminal oxidation; Krebs cycle; mitochondrial aconitase; zinc transport; apoptosis
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Funding
- NCI NIH HHS [R01 CA079903, CA79903, CA 71207, R01 CA071207] Funding Source: Medline
- NIDDK NIH HHS [R01 DK042839, DK42838, DK28015] Funding Source: Medline
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Human prostate secretory epithelial cells have the uniquely specialized function of accumulating and secreting extremely high levels of citrate. This is achieved by their ability to accumulate high cellular levels of zinc that inhibit citrate oxidation. This process of net citrate production requires unique metabolic/bioenergetic mitochondrial relationships. In prostate cancer, the malignant cells undergo a metabolic transformation from zinc-accumulating citrate-producing sane cells to citrate-oxidizing malignant cells that lost the ability to accumulate zinc. This review describes the metabolic/bioenergetic, zinc and mitochondrial relationships involved in normal and malignant prostate. Hopefully, this report will generate much needed interest and research in this neglected, but critically important, area of investigation. (C) 2005 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
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