Abstract |
The present work was set to study how CoQ concentrations affected steady-state levels of superoxide in a cellular model of partial CoQ(10) deficiency in cultured human myeloid leukemia HL-60 cells. Culturing HL-60 cells in the presence of p-aminobenzoate, a competitive inhibitor of polyprenyl-4-hydroxybenzoate transferase (Coq2p), produced a significant decrease of CoQ(10) levels without affecting cell viability. Concomitant decreases in CoQ-dependent electron transport activity and mitochondrial membrane potential were observed under these conditions. Intracellular superoxide was significantly elevated in cells treated with p-aminobenzoate, both under serum-containing and serum-free conditions, and this effect was reversed by exogenous CoQ(10). A slight increase of superoxide was also observed in CoQ(10)-supplemented cells in the absence of serum. Our results support a requirement for CoQ(10) to control superoxide levels in HL-60 cells. The importance of extramitochondrial sources of superoxide in cells with impaired CoQ(10) biosynthesis is discussed.
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Authors | David González-Aragón, María I Burón, Guillermo López-Lluch, María D Hermán, Consuelo Gómez-Díaz, Plácido Navas, José M Villalba |
Journal | BioFactors (Oxford, England)
(Biofactors)
Vol. 25
Issue 1-4
Pg. 31-41
( 2005)
ISSN: 0951-6433 [Print] Netherlands |
PMID | 16873928
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Coenzymes
- Phenanthridines
- Superoxides
- Ubiquinone
- hydroethidine
- Succinate Cytochrome c Oxidoreductase
- Alkyl and Aryl Transferases
- 4-hydroxybenzoate polyprenyltransferase
- coenzyme Q10
- 4-Aminobenzoic Acid
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Topics |
- 4-Aminobenzoic Acid
(pharmacology)
- Alkyl and Aryl Transferases
(antagonists & inhibitors)
- Coenzymes
- HL-60 Cells
- Humans
- Phenanthridines
(metabolism)
- Succinate Cytochrome c Oxidoreductase
(metabolism)
- Superoxides
(metabolism)
- Ubiquinone
(analogs & derivatives, deficiency, physiology)
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