Au Electrodeposition at the Liquid-Liquid Interface: mechanistic aspects

The deposition mechanism of metallic gold was investigated based on charge transfer voltammetry at the water/1,2-dichloroethane (W/DCE) interface, and the corresponding redox voltammetry of the metal precursor in W and the reductant, triphenylamine (TPA), in DCE. The metal precursor was present as Au(III) (AuCl_4^[−]), or Au(I) (AuCl_2^[−]) in W or DCE. Electron transfer could be observed voltammetrically at the interface between W containing both Au precursors and DCE containing TPA. Au particles, formed by constant potential electrolysis at the W/DCE interface, were examined by transmission electron microscopy. It was shown that deposit size could be controlled via the applied potential and time, with specific conditions to form particles of less than 10 nm identified

Electrochemical Insight into the Brust-Schiffrin Synthesis of Au Nanoparticles

The mechanism of the Brust–Schiffrin gold nanoparticle synthesis has been investigated through the use of ion transfer voltammetry at the water/1,2-dichloroethane (DCE) solution interface, combined with X-ray absorption fine structure (XAFS) of the reaction between [AuCl4]− and thiol (RSH) in homogeneous toluene (TL) solution. Ion transfer calculations indicate the formation of [AuCl2]− at RSH/Au ratios from 0.2–2 with a time-dependent variation observed over several days. At RSH/Au ratios above 2 and after time periods greater than 24 h, the formation of Au(I)SR is also observed. The relative concentrations of reaction products observed at the liquid/liquid interface are in excellent agreement with those observed by XAFS for the corresponding reaction in a single homogeneous phase. BH4– ion transfer reactions between water and DCE indicate that the reduction of [AuCl4]− or [AuCl2]− to Au nanoparticles by BH4– proceeds in the bulk organic phase. On the other hand, BH4– was unable to reduce the insoluble [Au(I)SR]n species to Au nanoparticles. The number and size of the nanoparticles formed was dependent on the concentration ratio of RSH/Au, as well as the experimental duration because of the competing formation of the [Au(I)SR]n precipitate. Higher concentrations of nanoparticles, with diameters of 1.0–1.5 nm, were formed at RSH/Au ratios from 1 to 2

Conjugated docosahexaenoic acid suppresses KPL-1 human breast cancer cell growth in vitro and in vivo: potential mechanisms of action

Introduction The present study was conducted to examine the effect of conjugated docosahexaenoic acid (CDHA) on cell growth, cell cycle progression, mode of cell death, and expression of cell cycle regulatory and/or apoptosis-related proteins in KPL-1 human breast cancer cell line. This effect of CDHA was compared with that of docosahexaenoic acid (DHA). Methods KPL-1 cell growth was assessed by colorimetric 3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay; cell cycle progression and mode of cell death were examined by flow cytometry; and levels of expression of p53, p21Cip1/Waf1, cyclin D1, Bax, and Bcl-2 proteins were examined by Western blotting analysis. In vivo tumor growth was examined by injecting KPL-1 cells subcutaneously into the area of the right thoracic mammary fat pad of female athymic mice fed a CDHA diet. Results CDHA inhibited KPL-1 cells more effectively than did DHA (50% inhibitory concentration for 72 hours: 97 μmol/l and 270 μmol/l, respectively). With both CDHA and DHA growth inhibition was due to apoptosis, as indicated by the appearance of a sub-G1 fraction. The apoptosis cascade involved downregulation of Bcl-2 protein; Bax expression was unchanged. Cell cycle progression was due to G0/G1 arrest, which involved increased expression of p53 and p21Cip1/Waf1, and decreased expression of cyclin D1. CDHA modulated cell cycle regulatory proteins and apoptosis-related proteins in a manner similar to that of parent DHA. In the athymic mouse system 1.0% dietary CDHA, but not 0.2%, significantly suppressed growth of KPL-1 tumor cells; CDHA tended to decrease regional lymph node metastasis in a dose dependent manner. Conclusion CDHA inhibited growth of KPL-1 human breast cancer cells in vitro more effectively than did DHA. The mechanisms of action involved modulation of apoptosis cascade and cell cycle progression. Dietary CDHA at 1.0% suppressed KPL-1 cell growth in the athymic mouse system.</p