Vitamin C versus Cancer: Ascorbic Acid Radical and Impairment of Mitochondrial Respiration?

Figure 1

“Protective mode” of action of the OMM Cyb5R3/VDAC1 at low (steady-state) concentrations of vitamin C in normal cells (at normoxia). OMM Cyb5R3/VDAC1 converts ascorbyl free radical (AFR; Asc^⋅-) to ascorbate (AscH^-), using cytosolic NADH as an electron donor. This prevents effects on mitochondrial respiration and all complexes operate in a “normal mode,” creating a proton gradient and leading to normal ATP synthesis. The CoQ “pool” is balanced [39], and the Qo site of Complex III transfers one electron to cytochrome c and the second electron to ubiquinone in the Qi site. VDAC1: voltage-dependent anion channel 1; Cyb5R3: NADH:cytochrome b5 oxidoreductase 3; OMM: outer mitochondrial membrane; Cyt. c: cytochrome c.