Antioxidant Deactivation on Graphenic Nanocarbon Surfaces

Abstract

This article reports a direct chemical pathway for antioxidant deactivation on the surfaces of carbon nanomaterials. In the absence of cells, carbon nanotubes are shown to deplete the key physiological antioxidant glutathione (GSH) in a reaction involving dissolved dioxygen that yields the oxidized dimer, GSSG, as the primary product. In both chemical and electrochemical experiments, oxygen is only consumed at a significant steady-state rate in the presence of both nanotubes and GSH. GSH deactivation occurs for single- and multi-walled nanotubes, graphene oxide, nanohorns, and carbon black at varying rates that are characteristic of the material. The GSH depletion rates can be partially unified by surface area normalization, are accelerated by nitrogen doping, and suppressed by defect annealing or addition of proteins or surfactants. We propose that dioxygen reacts with active sites on graphenic carbon surfaces to produce surface-bound oxygen intermediates that react heterogeneously with glutathione to restore the carbon surface and complete a catalytic cycle. The direct catalytic reaction between nanomaterial surfaces and antioxidants may contribute to oxidative stress pathways in nanotoxicity, and the dependence on surface area and structural defects suggest strategies for safe material design.

Reduced graphene oxide-catalyzed oxidative coupling reaction of 4-methoxyphenol in aerobic aqueous solution

“…rGOs do not typically act as oxidants [19], so we examined the effect of DO on the oxidation of MOP in the presence of rGOs (Fig. 4).…”

“…It seems unlikely for DO to participate in the oxidative reaction by direct fourelectron-transfer according to a previous research [19]. To decipher which ROS was responsible for the MOP coupling reaction, we examined the oxidative reaction of MOP through addition of SOD to catalyze disproportionation of superoxide anion (O 2 d ) or TBA to destroy hydroxyl radical ( OH) prior to sample incubation.…”

“…5, the addition of either SOD or TBA partially inhibited the coupling reaction of MOP, providing evidence that superoxide species and OH were formed in the MOP/rGO/O 2 system. In the previous research [19,49,50], it was suggested that DO can react with the defective sites on graphenic carbon surface to produce surface-bound ROS, primarily adsorbed (O 2 d ) ads . As a precursor of other ROS, (O 2 d ) ads had high reactivity.…”

“…This result was supported by previous studies. For example, Liu et al studied the oxidative coupling of glutathione in water, and found that the structural defect region on carbon nanotubes was the main active sites [19]. Similarly, it was showed that the defect sites in rGO were able to effectively activate peroxymonosulfate to produce active sulfate radicals, which promoted the decomposition of phenol, chlorophenols, dyes [16] and bisphenols [17].…”

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

“…7 Moreover, oxidative stress is believed to be a major toxic response to GO at toxic doses, and the generation of reactive oxygen species (ROS) is considered its main factor. 2,[8][9][10] The blood-brain barrier (BBB) has an intricate physical and molecular structure that provides the proper microenvironment for neuronal cell activity to withstand the penetration of foreign matter, including graphene materials. However, in recent decades, the penetration of materials through the BBB, especially nanomaterials, has become possible due to their tiny size.…”