Detecting the acellular oxidative reactivity of nanoparticles v1

This protocol was designed to detect acellular oxidative reactivity of nanoparticles

Base dependent 1,3-dithioacetals rearrangement over sulfoxidation under visible-light photocatalysis to access disulfide-linked-dithioesters

Base dependent oxidative rearrangement of dithiolanes and dithianes to access disulfide-linked-dithioesters under visible-light photoredox catalytic conditions has been disclosed. The protocol demonstrated the ability to synthesize either rearranged product or sulfoxide by simply switching the base with inherent ability to make hydrogen bonding with sulfur atom. Unlike, the usual deprotection of thioacetals to corresponding aldehydes under the oxidative conditions, we observed the unique regioselective oxidative reactivity of thioacetals to form disulfide-linked-dithioester or sulfoxides. The generality of the protocol has been demonstrated by exploring a wide range of substrates. As an application the in-situ generated thyil radical has been trapped with disulfides to prepare hetro-disulfides of potential utility. The protocol proved to be practical on gram scale quantity and relied on clean energy source for the transformation. Based on the series of control experiments, cyclic volametry and Stern-Volmer studies the plausible mechanism has been proposed.

Cytotoxicity Induction by the Oxidative Reactivity of Nanoparticles Revealed by a Combinatorial GNP Library with Diverse Redox Properties

It is crucial to establish relationship between nanoparticle structures (or properties) and nanotoxicity. Previous investigations have shown that a nanoparticle’s size, shape, surface and core materials all impact its toxicity. However, the relationship between the redox property of nanoparticles and their toxicity has not been established when all other nanoparticle properties are identical. Here, by synthesizing an 80-membered combinatorial gold nanoparticle (GNP) library with diverse redox properties, we systematically explored this causal relationship. The compelling results revealed that the oxidative reactivity of GNPs, rather than their other physicochemical properties, directly caused cytotoxicity via induction of cellular oxidative stress. Our results show that the redox diversity of nanoparticles is regulated by GNPs modified with redox reactive ligands.

Oxidase Reactivity of CuII Bound to N-Truncated Aβ Peptides Promoted by Dopamine

The redox chemistry of copper(II) is strongly modulated by the coordination to amyloid-β peptides and by the stability of the resulting complexes. Amino-terminal copper and nickel binding motifs (ATCUN) identified in truncated Aβ sequences starting with Phe4 show very high affinity for copper(II) ions. Herein, we study the oxidase activity of [Cu–Aβ4−x] and [Cu–Aβ1−x] complexes toward dopamine and other catechols. The results show that the CuII–ATCUN site is not redox-inert; the reduction of the metal is induced by coordination of catechol to the metal and occurs through an inner sphere reaction. The generation of a ternary [CuII–Aβ–catechol] species determines the efficiency of the oxidation, although the reaction rate is ruled by reoxidation of the CuI complex. In addition to the N-terminal coordination site, the two vicinal histidines, His13 and His14, provide a second Cu-binding motif. Catechol oxidation studies together with structural insight from the mixed dinuclear complexes Ni/Cu–Aβ4−x reveal that the His-tandem is able to bind CuII ions independently of the ATCUN site, but the N-terminal metal complexation reduces the conformational mobility of the peptide chain, preventing the binding and oxidative reactivity toward catechol of CuII bound to the secondary site.