Coenzyme Q and the regulation of intracellular steady-state levels of superoxide in HL-60 cells

The present work was set to study how CoQ concentrations affected steady‐state levels of superoxide in a cellular model of partial CoQ10 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‐hydrox...

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Bibliographic Details
Published in:BioFactors (Oxford) 2005, Vol.25 (1-4), p.31-41
Main Authors: González-Aragón, David, Burón, María I., López-Lluch, Guillermo, Hermán, María D., Gómez-Díaz, Consuelo, Navas, PlÁCido, Villalba, José M.
Format: Article
Language:English
Subjects:
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
Ubiquinone - deficiency
Ubiquinone - physiology
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Summary:The present work was set to study how CoQ concentrations affected steady‐state levels of superoxide in a cellular model of partial CoQ10 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 CoQ10 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 CoQ10. A slight increase of superoxide was also observed in CoQ10‐supplemented cells in the absence of serum. Our results support a requirement for CoQ10 to control superoxide levels in HL‐60 cells. The importance of extramitochondrial sources of superoxide in cells with impaired CoQ10 biosynthesis is discussed.
ISSN:0951-6433
1872-8081
DOI:10.1002/biof.5520250105