We report on a system of surface-enhanced Raman scattering (SERS) using solution-phase Ag decorated CuO nanoparticles. The Ag/CuO nanocomposite exhibits up to a 10 5 Raman signal enhancement as determined using the target molecule 4-aminothiophenol (4-ATP) at concentrations down to 10 μM. The surface plasmon absorption of Ag shifted slightly toward higher binding energy, which is attributed to electron transfer (charge transfer) from Ag to CuO. Further, metallic particles deposited on semiconductor materials formed a local electromagnetic field which altered the interfacial charge distribution. Using solution-phase SERS detection, the dynamic hot spot density was increased significantly, allowing for highly efficient analyte adsorption onto the Ag/CuO nanocomposite with increased electromagnetic field. The observed SERS signal enhancement in this solution-phase Ag/CuO nanocomposite system is attributed to a combination of chemical charge-transfer effect and electromagnetic enhancement occurring simultaneously at the metal−semiconductor interface. Because SERS detection is performed in the solution phase, this method provides a system for in-situ detection in aqueous environment and is thus well suited for monitoring analyte concentrations.

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Di-(2-ethylhexyl) phthalate (DEHP), the common plasticizer used in the production of polyvinyl chloride, can be converted to the more potent metabolite mono-ethylhexyl phthalate (MEHP). Epidemiological studies have shown an association with elevated induction of rat hepatic cancer and reproductive toxicity in response to MEHP exposure. However, the mechanism of genotoxicity and carcinogenicity induced by MEHP treatment remains unclear. As a means to elucidate the mechanisms of action, lethality and mutagenicity in the adenine phosphoribosyltransferase (aprt+/-) gene induced in several CHO cell types by MEHP were assessed. Dose-response relationships were determined in the parental AA8 cell line, its nucleotide repair-deficient UV5 and base repair-deficient EM9 subclones, and also in AS52 cells harboring the bacterial guanine-hypoxanthine phosphoribosyltransferase (gpt) gene and its derived AS52-XPD-knockdown and AS52-PARP-1-knockdown cells. Treatment of AS52 with MEHP led to intracellular production of reactive oxygen species (ROS) and DNA strand breaks in a dose-dependent manner. Separately, mutations in the gpt gene of AS52 cells were characterized and found to be dominated by G:C to A:T and A:T to G:C transitions. Independent AS52-mutant cell (ASMC) clones were collected for the sequential in vivo xenograft tumorigenic studies, 4 of total 20 clones had aggressive tumor growth. Moreover, microarray analysis indicated miR-let-7a and miR-125b downregulated in ASMC, which might raise oncogenic MYC and RAS level and activate ErbB pathway. Comparative evaluation of the results indicates that the principal mechanism of this mutagenic action is probably to be through generation of ROS, causing base excision damage resulting in carcinogenicity.

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