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A polyacrylic acid (PAA)-protected platinum nanoparticle species (PAA-Pt) was prepared by alcohol reduction of hexachloroplatinate. The PAA-Pt nanoparticles were well dispersed and homogeneous in size with an average diameter of 2.0 +/- 0.4 nm (n = 200). We used electron spin resonance to quantify the residual peroxyl radical ([Formula: see text]) generated from 2,2-azobis (2-aminopropane) dihydrochloride (AAPH) by thermal decomposition in the presence of O(2) and a spectrophotometric method to quantify the residual 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical. PAA-Pt scavenged these two radicals in a dose-dependent manner. Platinum was the functional component. PAA-Pt reduced the rate of oxygen consumption required for linoleic acid peroxidation initiated by [Formula: see text] generated from AAPH, indicating inhibition of the propagation of linolate peroxidation. A thiobarbituric acid test also revealed dose-dependent inhibition of the linolate peroxidation by PAA-Pt. Fifty micromolar platinum, as PAA-Pt, completely quenched 250 microM DPPH radical for 5 min. Even when twice diluted in half, the PAA-Pt still quenched 100% of the 250 microM DPPH radical. The scavenging activity of PAA-Pt is durable. These observations suggest that PAA-Pt is an efficient scavenger of free radicals.

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MicroRNAs are known to be the important regulators of skin physiology and considered as new therapeutic targets to treat skin diseases. In this study, miR-125b was identified as a potent regulator of steady-state melanogenesis. We found that the expression of miR-125b was inversely related to pigment levels. A miR-125b mimic decreased the expression of pigmentation-related gene and melanin content, implying that miR-125b functions to decrease pigmentation. Moreover, we observed that the reduction in miR-125b expression in pigmented cells was at least partially due to the hypermethylation of the MIR125B-1 promoter, and miR-125b expression was regulated by intracellular cAMP levels.