Three manganesecarbonyl complexes having a xanthenebased silane(silyl) or bis(silyl) chelate ligand were synthesized and characterized. The single-crystal X-ray analysis of these complexes demonstrated that an SiH bond is sequentially activated on the metal according to ligand substitution of CO with xanthene-oxygen or η 6 -toluene.The SiH bond activation of hydrosilanes induced by transition-metal complexes is an attractive process for its broad application to the synthesis of organosilicon compounds (e.g., hydrosilylation).1 Generally, it is proposed that this bond activation can be achieved by interaction of the SiH · bond with a coordinatively unsaturated metal center.1 A possible reaction mechanism of the SiH activation suggested by Schubert and co-workers based on their comprehensive study (Scheme 1) involves the generation of silane complexes A and B, both having a 3c2e MHSi bond, as key intermediates.

Ruthenium complexes bearing a xanthene-based bis­(silyl) chelate ligand, “xantsil” ((9,9-dimethylxanthene-4,5-diyl)­bis­(dimethylsilyl)), Ru­{κ3(Si,O,Si)-xantsil}­(CO)­(PR3) (1-Cy: R = Cy (cyclohexyl), 1-Cyp: R = Cyp (cyclopentyl)), were found to catalyze the reactions of internal arylalkynes with tertiary silanes (1–1.3 equiv) at a moderate temperature (room temperature to 70 °C) to give (E)-alkenes having an ortho-silylated aryl group, i.e., (E)-R1C­(H)C­(H)­(C6H3-o-SiR3 3-p-R2). These catalytic reactions involve a unique ortho-selective C–H silylation of an aryl group in arylalkynes accompanied by hydrogenation of their C–C triple bonds (ortho-C–H silylation/hydrogenation). Importantly, in these reactions, the alkynyl moiety of arylalkynes serves as both a directing group and a hydrogen acceptor. The substrate scope of this ortho-C–H silylation/hydrogenation was explored by use of eight combinations of arylalkynes and tertiary silanes. In cases using bulky substrates, the catalytic performance of 1-Cyp with a relatively less bulky phosphine ligand (PCyp3) was shown to be superior to that of the PCy3 analogue 1-Cy.

We examined drug concentrations and the incidence of retinal degeneration in the eyes of albino BALB/c mice after a single intravenous administration of sitafloxacin plus a 4 h period of UVA irradiation. Retinal degeneration was induced at 40 mg/kg or more plus UVA irradiation, and there was little decrease in ocular sitafloxacin concentration under UVA irradiation. We then examined the incidence of retinal degeneration with various periods of UVA irradiation in BALB/c mice given a single intravenous administration of 40 mg/kg sitafloxacin. Retinal degeneration occurred in all the groups receiving UVA irradiation immediately after sitafloxacin administration, whereas no retinal degeneration occurred in the groups receiving UVA irradiation starting 30 min or later after administration. In addition, we examined both the retinal degeneration and auricular inflammation in BALB/c mice given a 7-day repeated administration of sitafloxacin at 1, 3.3 and 10 mg/kg per day, which never induce retinal or auricular change by a single administration. Retinal degeneration was not induced at any dose level, although auricular skin inflammation was augmented by repeated administration. These results suggest that the occurrence of retinal degeneration depends on maximum ocular sitafloxacin concentration during UVA irradiation, whereas the severity of auricular inflammation is directly proportional to the total decrease in area under the drug concentration curve for auricular sitafloxacin under UVA irradiation. This difference between retinal degeneration and auricular inflammation may derive from their respective mechanisms of pathogenesis.