Among various metal ions of physiological interest, Cu2+ is uniquely capable of catalyzing the oxidation of NADH by H2O2. This oxidation is stimulated about fivefold in the presence of imidazole. A similar activating effect is found for some imidazole derivatives (1-methyl imidazole, 2-methyl imidazole, andN-acetyl-L-histidine). Some other imidazole-containing compounds (L-histidine,L-histidine methyl ester, andL-carnosine), however, inhibit the Cu2+-catalyzed peroxidation of NADH. Other chelating agents such as EDTA andL-alanine are also inhibitory. Stoichiometry for NADH oxidation per mole of H2O2 utilized is 1, which excludes the possibility of a two-step oxidation mechanism with a nucleotide free-radical intermediate. About 92% of the NADH oxidation product can be identified as enzymatically active NAD+. D2O, 2,5-dimethylfuran, and 1,4-diazabicyclo [2.2.2]-octane have no significant effect on the oxidation, thus excluding1O2 as a mediator. Similarly, OH· is also not a likely intermediate, since the system is not affected by various scavengers of this radical. The results suggest that a copper-hydrogen peroxide intermediate, when complexed with suitable ligands, can generate still another oxygen species much more reactive than its parent compound, H2O2.
Copper (II) complex, as catalyst in H2O2 oxidation of NADH catalyst, Cu (II) in H2O2 oxidation of NADH hydrogen peroxide, Cu (II) catalysis of NADH oxidation by NADH, oxidation by Cu (II) complex and H2O2oxidation, of NADH by Cu (II) catalyzed H2O2
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