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

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Abstract
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.