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 H(2)PtCl(6) 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 microM 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 3h was approximately 20 microM, 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 (CoQ(1)) was observed by incubating CoQ(1) with CP-Pt in an aqueous buffer. A further analysis with HPLC revealed the reduction of CoQ(1) to CoQ(1)H(2) 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.