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Research was conducted to examine biomimetic alkane hydroxylations by an iron(III) porphyrin complex with H2O2 and by a high-valent iron(IV) oxo porphyrin cation radical complex. Results demonstrate that an electronegatively-substituted iron porphyrin complex efficiently catalyzes the hydroxylation of alkanes by H2O2 via radical-free oxidation reactions in aprotic solvvent and that an isolated high-valent iron(IV) oxo porphyrin cation radical intermediate of the iron porphyrin complex can activate C-H bonds of alkanes to give oxygenated products efficiently at low temperatures.

The luminescent characteristics of Ru(bpy)[sub2]dppz[sup2+] (dppz = dipyrido[3,2-a:2',3'-cjphenazine), a DNA light switch, were investigated in the presence of oligonucleotides containing single base mismatches or an abasic site. In water, the ruthenium luminescence is quenched, but, bound to well matched duplex DNA, the Ru complex luminesces. Here we show that with DNAs containing a defect, rae-, Δ-, and Λ-Ru(bpy)[sub2]dppz[sup2+] exhibit significant luminescent enhancements above that with well matched DNA. In the presence of a single base mismatch, large luminescent enhancements are evident for the Δ-Ru isomer; the Λ-isomer shows particularly high luminescence bound to an oligonucleotide containing an abasic site. Similar increases are not evident with two common DNA-binding organic fluorophores, ethidium bromide and TO-PRO-3. Titrations with hairpin oligonucleotides containing a variable mismatch site show correlation between the level of luminescent enhancement and the thermodynamic destabilization associated with the mismatch. This correlation is reminiscent of that found earlier for a bulky rhodium complex that binds mismatched DNA sites through metalloinsertion, where the complex binds the DNA from the minor groove side, ejecting the mismatched bases into the major groove. Differential qubnching studies with minor and major groove quenchers and time-resolved emission studies support this metalloinsertion mode for the dppz complex at the defect site. Certainly these data underscore the utility of Ru(bpy)[sub2]dppz[sup2+] as a sensitive luminescent reporter of DNA and its defects. [ABSTRACT FROM AUTHOR]

Amyloid-beta (Abeta) plaques are largely associated with the neuropathogenesis of Alzheimer's disease (AD). Metal ions such as Cu(II) and Zn(II) have been implicated as contributors to their formation and deposition. Metal chelators have been used to modulate metal-induced Abeta aggregation. The bidentate ligand clioquinol (CQ) presents an effective influence on metal-involved Abeta aggregation, which has been explained through its metal chelation and is generally monitored by fluorescence and turbidity assays in vitro. The studies herein, however, suggest that the effects of CQ on metal-driven Abeta aggregation may not be visualized accurately by both assays. Subsequently, the present work demonstrates that CQ is able to chelate metal ions from metal-Abeta species and to assist, in part, in the disaggregation of Abeta aggregates, but it could not completely hinder the progression of Abeta aggregation.

The luminescent characteristics of Ru(bpy)(2)dppz(2+) (dppz = dipyrido[3,2-a:2',3'-c]phenazine), a DNA light switch, were investigated in the presence of oligonucleotides containing single base mismatches or an abasic site. In water, the ruthenium luminescence is quenched, but, bound to well matched duplex DNA, the Ru complex luminesces. Here we show that with DNAs containing a defect, rac-, Delta-, and Lambda-Ru(bpy)(2)dppz(2+) exhibit significant luminescent enhancements above that with well matched DNA. In the presence of a single base mismatch, large luminescent enhancements are evident for the Delta-Ru isomer; the Lambda-isomer shows particularly high luminescence bound to an oligonucleotide containing an abasic site. Similar increases are not evident with two common DNA-binding organic fluorophores, ethidium bromide and TO-PRO-3. Titrations with hairpin oligonucleotides containing a variable mismatch site show correlation between the level of luminescent enhancement and the thermodynamic destabilization associated with the mismatch. This correlation is reminiscent of that found earlier for a bulky rhodium complex that binds mismatched DNA sites through metalloinsertion, where the complex binds the DNA from the minor groove side, ejecting the mismatched bases into the major groove. Differential quenching studies with minor and major groove quenchers and time-resolved emission studies support this metalloinsertion mode for the dppz complex at the defect site. Certainly these data underscore the utility of Ru(bpy)(2)dppz(2+) as a sensitive luminescent reporter of DNA and its defects.