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In solution, unsubstituted guanine (GH2) is in a tautomeric equilibrium between 1H,7H-keto and 1H,9H-keto forms. Upon coordination with (dien)PtII, N9-bound mononuclear complex is preferentially formed. With excess (dien)PtII, the dinuclear complex [{Pt(dien)}2(GH-N7,N9)]3+is formed at basic pH. The X-ray crystal structure analysis of mononuclear complexes [Pt(dien)(GH2-N9)](ClO4)2·2.25H2O (1a), [Pt(dien)(GH2-N9)](Cl)(ClO4) (1b), and the dinuclear complex [{Pt(dien)}2(GH-N7,N9)](ClO4)3(3) are reported. The N7 linkage isomer [Pt(dien)(GH2-N7)]2+(2) could not be isolated and was tentatively assigned in solution. In HCl-acidic medium, the dinuclear complex 3dissociates to form N9 bound mononuclear complex (1) as the major product and presumably the N7 linkage isomer (2) as a minor side product. Species 1and 3have been identified by the pD dependence of the 1H NMR guanine resonances. pKavalues (calculated for H2O) for deprotonation of the N9 linkage isomer (1a, 1b) are 6.51 ± 0.01 and 10.53 ± 0.05 as well as 0.52 ± 0.07 and 8.55 ± 0.06 for the dinuclear complex [{Pt(dien)}2(GH-N7,N9)]3+(3). Ab initiocalculations have been performed for [Pt(dien)(GH2-N7)]2+, [Pt(dien)(GH2-N9)]2+and [{Pt(dien)}2(GH-N7,N9)]3+. They reveal that in gas phase the N7 linkage isomer is more stable than the N9 linkage isomer by ΔE= 8.4 kcal mol−1. Reactions with (dien)PtIIand cis-(NH3)2PtIIwere also carried out to study the metal binding behaviour of the ligand, 7-methylguanine (7-MeGH). The complexes [Pt(dien)(7-MeGH-N9)](NO3)(ClO4) (4), cis-[Pt(NH3)2(7-MeGH-N9)2]Cl2·2H2O (5) and cis,cis-[{PtCl(NH3)2}2(7-MeGH-N3,N9)]Cl2·3H2O (6) have been characterized by X-ray crystallography. pKavalues for 4are < 2 and 8.16 ± 0.04, and for 51.86 ± 0.45 and 8.00 ± 0.08 (average for deprotonation of two 7-MeGH ligands). Structural peculiarities of N9 platinated guanine ligands are discussed and pKavalues of Pt complexes with related guanine nucleobases are compared. [ABSTRACT FROM AUTHOR]

The decomposition of peroxynitrite near neutral pH leads ultimately to the formation of dioxygen and nitrite viaan intermediate with an absorbance maximum at 284 nm. The intermediate oxidises I−with a rate constant of (78 ± 8) × 10 M−1s−1and decays near pH 7 with a rate constant of (0.58 ± 0.02) s−1at 22 °C, but is longer-lived at lower pH. On the basis of experiments performed with a tandem-quenching flow reactor, we tentatively identify this intermediate as peroxynitric acid, formed during the proposed reaction sequence ONOOH + ONOO−→ NO2−+ O2NOO−+ H+→ 2 NO2−+ O2. These products are those expected from a peracid. The rate constant for the first reaction is ca.3 × 104M−1s−1. Part of the dioxygen formed is in the 1Δgstate (S. Miyamoto, G. E. Ronsein, T. C. Corréa, G. R. Martinez, M. H. G. Medeiros and P. Di Mascio, Dalton Trans., 2009, DOI: 10.1039/b905560f). The decay of peroxynitrous acid at concentrations higher than 0.1 mM near neutral pH is best described by the simultaneous process of isomerisation (k= 1.2 s−1) and decomposition to peroxynitrate. The rate of formation and the amount of peroxynitrate formed are much larger than can be accounted for by homolysis reactions. [ABSTRACT FROM AUTHOR]

Metal binding to ligands with the potential of existing in different tautomeric structures can dramatically alter the tautomeric equilibrium by stabilizing a particular, frequently minor, tautomer. The assumption that metal complexation of a minor tautomer is chemically irrelevant because of its very low abundance is misleading and in many cases wrong. In fact, from available X-ray structural data on metal–nucleobase complexes it is evident that metal binding to rare, as opposed to preferred tautomers, is anything but an exception. This “promotion of rare tautomers” through metal coordination is of particular biological relevance in the case of nucleobases because any deviation from Watson–Crick base pairing is potentially mutagenic. In recent years models of “metal-stabilized rare nucleobase tautomers” have been characterized for all common DNA nucleobases, including by X-ray crystallography. Though metal binding causes relatively minor structural changes in the nucleobases, electronic changes as expressed by acid–base properties, for example, can be substantial. In this perspective article the biological consequences of the occupation of nucleobase sites by a metal entity and the altered acid–base chemistry of the nucleobase with regard to base mismatch formation, prevention of base pairing, and acid–base catalysis in nucleic acids are examined. Although not relevant to biology, the behaviour of the unsubstituted parent nucleobases is illuminating in this respect and therefore included. [ABSTRACT FROM AUTHOR]