Bimetallic nanoparticles consisting of gold and platinum were prepared by a citrate reduction method and complementarily stabilized with pectin (CP-Au/Pt). The percent mole ratio of platinum was varied from 0 to 100%. The CP-Au/Pt were alloy-structured. They were well dispersed in water. The average diameter of platinum nanoparticles (CP-Pt) was 4.7 +/- 1.5 nm. Hydrogen peroxide (H(2)O(2)) was quenched by CP-Au/Pt consisting of more than 50% platinum whereas superoxide anion radical (O(2)(-)) was quenched by any CP-Au/Pt. The CP-Au/Pt quenched these two reactive oxygen species in dose-dependent manners. The CP-Pt is the strongest quencher. The CP-Pt decomposed H(2)O(2) and consequently generated O(2) like catalase. The CP-Pt actually quenched O(2)(-) which was verified by a superoxide dismutase (SOD) assay kit. This quenching activity against O(2)(-) persisted like SOD. Taken together, CP-Pt may be a SOD/catalase mimetic which is useful for medical treatment of oxidative stress diseases.

Cancer cells have a unique energy metabolism for sustaining rapid proliferation. The preference for anaerobic glycolysis under normal oxygen conditions is a unique trait of cancer metabolism and is designated as the Warburg effect. Enhanced glycolysis also supports the generation of nucleotides, amino acids, lipids, and folic acid as the building blocks for cancer cell division. Nicotinamide adenine dinucleotide (NAD) is a co-enzyme that mediates redox reactions in a number of metabolic pathways, including glycolysis. Increased NAD levels enhance glycolysis and fuel cancer cells. In fact, nicotinamide phosphoribosyltransferase (Nampt), a rate-limiting enzyme for NAD synthesis in mammalian cells, is frequently amplified in several cancer cells. In addition, Nampt-specific inhibitors significantly deplete NAD levels and subsequently suppress cancer cell proliferation through inhibition of energy production pathways, such as glycolysis, tricarboxylic acid (TCA) cycle, and oxidative phosphorylation. NAD also serves as a substrate for poly(ADP-ribose) polymerase (PARP), sirtuin, and NAD gylycohydrolase (CD38 and CD157); thus, NAD regulates DNA repair, gene expression, and stress response through these enzymes. Thus, NAD metabolism is implicated in cancer pathogenesis beyond energy metabolism and considered a promising therapeutic target for cancer treatment. In this review, we present recent findings with respect to NAD metabolism and cancer pathogenesis. We also discuss the current and future perspectives regarding the therapeutics that target NAD metabolic pathways.

Background: Nmnat3 is considered a mitochondria-localized NAD synthesis enzyme. However, its physiological function in vivo remains unclear. Results: Loss of Nmnat3 results in drastic depletion of the NAD pool and stalls the glycolytic flow in mature erythrocytes. Conclusion: Nmnat3 deficiency causes splenomegaly and hemolytic anemia in mice. Significance: This report reveals the essential role of Nmnat3 in mature erythrocytes.

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