Platinum nanoparticles have an activity similar to mitochondrial NADH:ubiquinone oxidoreductase

This study was designed to examine if platinum nanoparticles have an activity similar to mitochondrial complex I, NADH:ubiquinone oxidoreductase. Platinum nanoparticles were prepared by a citrate reduction of H2PtCl6 and protected by citrate itself and pectin (CP-Pt). Time- and dose-dependent decreases in NADH and a time-dependent increase in NAD+ were observed in the presence of 50 μM CP-Pt; these observations were made using a spectrophotometric method in which the maximum absorption spectra at 340 and 260 nm were used for NADH and NAD+, respectively. The required platinum concentration in CP-Pt to achieve a 50% oxidation of NADH for 3 h was approximately 20 μM, and this NADH oxidation did not require oxygen as an electron acceptor. We also verified NAD+ formation using an NAD+/NADH quantification kit. The absorption peak shift from 278 to 284 nm of 2,3-dimethoxy-5-methyl-6-(3-methyl-2-butenyl)-1,4-benzoquinone (CoQ1) was observed by incubating CoQ1 with CP-Pt in an aqueous buffer. A further analysis with HPLC revealed the reduction of CoQ1 to CoQ1H2 by CP-Pt. As a whole, platinum nanoparticles have an NADH:ubiquinone oxidoreductase-like activity. This suggests that platinum nanoparticles are a potential medicinal substance for oxidative stress diseases with suppressed mitochondrial complex I.