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Costello LC, Guan Z, Kukoyi B, et al. Terminal oxidation and the effects of zinc in prostate versus liver mitochondria. Mitochondrion. 2004;4(4):331-8doi: 10.1016/j.mito.2004.07.031.
Costello, L. C., Guan, Z., Kukoyi, B., Feng, P., & Franklin, R. B. (2004). Terminal oxidation and the effects of zinc in prostate versus liver mitochondria. Mitochondrion, 4(4), 331-8. https://doi.org/10.1016/j.mito.2004.07.031
Costello, Leslie C, et al. "Terminal oxidation and the effects of zinc in prostate versus liver mitochondria." Mitochondrion vol. 4,4 (2004): 331-8. doi: https://doi.org/10.1016/j.mito.2004.07.031
Costello LC, Guan Z, Kukoyi B, Feng P, Franklin RB. Terminal oxidation and the effects of zinc in prostate versus liver mitochondria. Mitochondrion. 2004 Aug;4(4):331-8. doi: 10.1016/j.mito.2004.07.031. PMID: 16120396; PMCID: PMC4464835.
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Mitochondrion. 2004 Aug;4(4):331-8. doi: 10.1016/j.mito.2004.07.031.

Terminal oxidation and the effects of zinc in prostate versus liver mitochondria.

Mitochondrion

Leslie C Costello, Zhixin Guan, Boone Kukoyi, Pei Feng, Renty B Franklin

Affiliations

  1. Department of Biomedical Sciences, Dental School--University of Maryland, 666 West Baltimore Street, Baltimore, MD 21201, USA. [email protected]

PMID: 16120396 PMCID: PMC4464835 DOI: 10.1016/j.mito.2004.07.031

Abstract

Although the total zinc content of cells generally approximates 0.2 mM, the cytosolic free zinc ion concentration is negligible (subnanomolar concentrations). However, all reported studies of effects of zinc on cellular respiration and terminal oxidation involved microM-mM levels of free zinc ions. Prostate cells and their mitochondria accumulate 3-10 fold more zinc than other mammalian cells. We considered that a cytosolic pool of mobile reactive low molecular weight zinc ligands could inhibit respiration and terminal oxidation. The effects of ZnLigands, especially ZnCitrate, versus free Zn++ ions on respiration and terminal oxidation were studied with prostate and liver mitochondria. ZnLigands were equally as effective as free Zn++ ions in the inhibition of respiration and terminal oxidation of both prostate and liver mitochondria, which supports our concept that zinc can be transferred from cytosolic donor ZnLigands directly to zinc-binding sites of terminal oxidation components. Also, the respiration and specific activities of terminal oxidation components of prostate mitochondria are 20-50% of liver mitochondria. Zinc inhibition and inherently low levels of electron transport components are likely major factors responsible for the low respiration that characterizes prostate cells.

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