The DNA nucleosides (dA, dC, dG, dT) bound to gold nanoparticles (~13 nm) in aqueous solution has been studied as a probe by the SERS and their coordination structures have been proposed on the basis of them. According to UV-Visible absorption of gold nanoparticles after modifying with DNA nucleosides, the rates of absorption of dA, dC, and dG were much faster than that of dT as monitored by the aggregation kinetics at 700 nm. These data indicated that the nucleosides dA, dC, and dG had a higher affinity for the gold nanoparticles surface than nucleoside dT. As the result of SERS spectra, the binding modes of each of the nucleosides on gold nanoparticles have been assigned. A dA binds to gold nanoparticles via a N(7) nitrogen atom of the imidazole ring, which the C(6)-NH2 group also participates in the coordination process. In the case of dC, it binds to the gold surface via a N(3) nitrogen atom of the pyrimidine ring with a partial contribution from the oxygen of C(2)=O group. A coordination of dG to the gold surfaces is also proposed. Although the dG has the two different nitrogens of a pyrimidine ring and the amino group, the N(1) nitrogen atom of a pyrimidine ring has a higher affinity after the hydrogen migrates to the amino group. Conversely, dT binds via the oxygen of the C(4)=O group of the pyrimidine ring. Accordingly, these data suggest that the nitrogen atom of the imidazole or the pyrimidine ring in the DNA nucleosides will bind more fast to the gold nanoparticles surfaces than the oxygen atom of the carbonyl group.

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The Coordination Chemistry of DNA Nucleosides on Gold Nanoparticles as a Probe by SERS

Hexavalent chromium (Cr (VI)) is reduced intracellularly to Cr (V), Cr (IV) and Cr (HI) by ascorbate (Asc), cysteine and glutathione (GSH). These metabolites induce a spectrum of genomic DNA damage resulting in the inhibition of DNA replication. Our previous studies have shown that treatment of DNA with Cr (III) or Cr (VI) plus Asc results in the formation of DNA-CrDNA crosslinks (Cr-DDC) and guanine-specific arrests of both prokaryotic and mammalian DNA polymerases. GSH not only acts as a reductant of Cr (VI) but also becomes crosslinked to DNA by Cr, thus, the focus of the present study was to examine the role of GSH in Cr-induced DNA damage and polymerase arrests. Co-incubation of Cr (III) with plasmid DNA in the presence of GSH led to the crosslinking of GSH to DNA. GSH co-treatment with Cr (III) also led to a decrease in the degree of Cr-induced DNA interstrand crosslinks relative to Cr(III)alone, without affecting total Cr DNA binding. DNA polymerase arrests were observed following treatment of DNA with Cr (III) alone, but were markedly reduced when GSH was added to the reaction mixture. Pre-formed polymerase-arresting lesions (Cr-DDC) were not removed by subsequent addition of GSH. Treatment of DNA with Cr (VI), in the presence of GSH, resulted in crosslinking of GSH to DNA, but failed to produce detectable DNA interstrand crosslinks or polymerase arrests. The inhibitory effect of GSH on Cr-induced polymerase arrest was further confirmed in human genomic DNA using quantitative PCR (QPCR) analysis. Treatment of genomic DNA with Cr (III) resulted in a marked inhibition of the amplification of a 1.6 kb target fragment of the p53 gene byTagpolymerase. This was almost completely prevented by co-treatment with GSH and Cr (III). These results indicate that Cr-induced DNA interstrand crosslinks, and not DNA-Cr-GSH crosslinks, are the principal lesions responsible for blocking DNA replication. Moreover, the formation of DNA-Cr-GSH crosslinks may actually preclude the formation of the polymerase arresting lesions. (Mol Cell Biochem222:173-182, 2001)

Effects of glutathione on chromium-induced DNA crosslinking and DNA polymerase arrest

Effects of dietary caffeine on renal handling of minerals in adult women.

Publisher Summary This chapter discusses the perchlorate ion complexes. Coordination of perchlorate to transition and nontransition metal ions has been well established, though in most of the cases the metal-perchlorate bond is rather weak and has been termed as “semicoordination”. The highly symmetrical perchlorate ion is a hard base and falls into the category of relatively nonpolarizable and noncoordinating anions such as BF 4 ˉ and PF 6 ˉ. Its ability to coordinate strongly to soft metal ions is therefore limited. When coordination does occur, the perchlorate group may be linked to a metal ion in a monodentate and/or bidentate manner through oxygen atoms; the latter linkage can be either chelating. X-ray crystal structure analysis has unequivocally established coordination of perchlorate in a number of perchlorate complexes.

Thu Ba Tran

Papers

Xanthine, hypoxanthine and guanine copper(II) complexes

Guanine complexes with first row transition metal perchlorates

Copper(II) perchlorate complexes with N-methyl substituted xanthines

Adennine N(1)-oxide complexes with first row transition metal perchlorates

Purine N(1)-oxide complexes with 3d metal perchlorates