ABSTRACT
DNA inhibits hydride transfer from 1-benzyl-1,4-dihydronicotinamide to the 10-methylacridinium ion, whereas DNA accelerates photoinduced electron transfer from the excited state of Ru(bpy)3(2+) to the 1-methylquinolinium ion. The reason of such reversed effects of DNA on the hydride transfer and electron transfer reactions is clarified.
Subject(s)
2,2'-Dipyridyl/analogs & derivatives , Acridines/chemistry , DNA/chemistry , Quinolines/chemistry , 2,2'-Dipyridyl/chemistry , Acridines/metabolism , Cations/chemistry , Coordination Complexes , Electron Transport , Hydrogen/chemistry , Oxidation-Reduction , Quinolines/metabolism , Ruthenium/chemistryABSTRACT
The possible application of polyhydroxyalkanoate (PHA) in transdermal drug delivery systems (TDDSs) for tamsulosin was previously reported. PHAs containing the drugs, ketoprofen, clonidine and tamsulosin showed good adhesiveness to the skin model used, that is, shed snake skin, and dispersed well all model drugs tested. The model drugs hardly permeated through snake skin in solution form. However, these drugs permeated well through snake skin from the PHA matrix. It was previously reported that the addition of a dendrimer, a polymeric permeation enhancer, is effective for the TDDS for tamsulosin to establish an effective clinical TDDS. The effect of dendrimer addition was examined in TDDSs for ketoprofen and clonidine. The dendrimer added did not show an enhancement effect on the TDDSs for the two drugs. To investigate the mechanism of the enhancement effect of a dendrimer on the tamsulosin TDDS, X-ray analyses were performed. With dendrimer addition, drug crystallization in PHA was promoted. The crystal in PHA had highly ordered and changed its space group. These findings are very important for exploiting high-performance PHA-based TDDSs.
