Abstract
Long-term treatment with ethidium bromide of HL-60 cells induced a mitochondria-deficient ρ° cell line, where mitochondrial DNA can not be identified by PCR and cytochromecoxidase activity was 80% decreased. These cells showed a progressive increase of ascorbate stabilization which was 52% higher in the established ρ°HL-60 cells. Both CoQ10and NADH-ascorbate free radical reductase of the plasma membrane were increased in ρ° HL-60 cells compared to parental cells, while NADH-cytochromecreductase was unchanged. CoQ10is a component of the ascorbate stabilization activity in the plasma membrane that would provide both a mechanism to deplete the excess of NADH produced in ρ° HL-60 cells and for resistance to oxidative stress.
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