We reported the reduction process of palladium(II) acetate, Pd(OAc) 2 , and the self-assembling process of the resulting palladium atoms, Pd(0), into nanoparticles in the presence of a first-generation polyamidoamine dendrimer (G1-NH 2 ) in nonaqueous solution. The process was induced by mixing the two solutions (A) Pd(OAc) 2 dissolved in N,N-dimethylformamide (DMF) and (B) G1-NH 2 dissolved in methanol, under the specific condition of r ≡ [Pd(OAc) 2 ]/[-NH 2 ] ) 3.3, where [-NH 2 ] is the molar concentration of the primary amine groups in the dendrimer in the reaction solution. The reaction and reaction-induced self-assembling process were explored in situ by means of a combined time-resolved method of small-angle neutron scattering and smallangle X-ray scattering. The method revealed the time evolution of a series of self-assembling processes occurring in the system. (a) The dendrimer molecules and Pd(OAc) 2 first self-assemble themselves rapidly into spherical aggregates with an average radius of ∼30 nm after onset of the reaction, and thereafter their size was kept almost constant. (b) Inside the aggregates, which serve as a template for the reaction, the reduction of Pd(OAc) 2 to Pd(0) and their self-assembly into Pd nanoparticles with an average radius of 0.4-1.7 nm proceeds gradually with time over 12 h. The following factors are proposed to be important for understanding the series of self-assembling processes: (i) the relative strength of interactions among the constituents Pd(OAc) 2 , G1-NH 2 , DMF, and methanol and (ii) the reduction of Pd(OAc) 2 with methanol as a weak reducing agent and the self-assembly of the reduction products of Pd(0) in the templates.
Malignant mesothelioma is an asbestos-related fatal disease with no effective cure. We studied whether a green tea polyphenol, epigallocathechin-3-gallate (EGCG), could induce cell death in five human mesothelioma cell lines. We found that EGCG induced apoptosis in all five mesothelioma cell lines in a dose-dependent manner. We further clarified the cell killing mechanism. EGCG induced reactive oxygen species (ROS), and impaired the mitochondrial membrane potential. As treatment with ROS scavengers, catalase and tempol, significantly inhibited the EGCG-induced apoptosis, ROS is considered to be responsible for the EGCG-induced apoptosis. Further, we found that EGCG induced autophagy, and that when autophagy was suppressed by chloroquine, the EGCG-induced cell death was enhanced. Taken together, these results suggest that EGCG has a great potential for the treatment of mesothelioma by inducing apoptosis and autophagy.
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