Affiliations: Departamento de Biología Celular, Fisiología
e Inmunología, Universidad de Córdoba, Córdoba, Spain | Centro Andaluz de Biologíza del Desarrollo,
Universidad Pablo de Olavide, Sevilla, Spain
Note: [] Address for correspondence: Dr. J.M. Villalba, Departamento de
Biología Celular, Fisiología e Inmunología, Facultad de
Ciencias, Universidad de Córdoba, Campus Rabanales, Edificio Severo
Ochoa, 3^a planta, 14014-Córdoba, Spain
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.
Journal: BioFactors, vol. 25, no. 1-4, pp. 31-41, 2005
