Faculty, Staff and Student Publications

Language

English

Publication Date

3-1-2024

Journal

Advanced Materials

DOI

10.1002/adma.202211241

PMID

37272655

PMCID

PMC10696138

PubMedCentral® Posted Date

3-1-2025

PubMedCentral® Full Text Version

Author MSS

Abstract

Hydrogen sulfide (H2S) is a noxious, potentially poisonous, but necessary gas produced from sulfur metabolism in humans. In Down Syndrome (DS), the production of H2S is elevated and associated with degraded mitochondrial function. Therefore, removing H2S from the body as a stable oxide could be an approach to reducing the deleterious effects of H2S in DS. In this report we describe the catalytic oxidation of hydrogen sulfide (H2S) to polysulfides (HS2+n−) and thiosulfate (S2O32−) by poly(ethylene glycol) hydrophilic carbon clusters (PEG-HCCs) and poly(ethylene glycol) oxidized activated charcoal (PEG-OACs), examples of oxidized carbon nanozymes (OCNs). We show that OCNs oxidize H2S to polysulfides and thiosulfate in a dose-dependent manner. The reaction is dependent on oxygen and the presence of quinone groups on the OCNs. In DS donor lymphocytes we found that OCNs increased polysulfide production, proliferation, and afforded protection against additional toxic levels of H2S compared to untreated DS lymphocytes. Finally, in Dp16 and Ts65DN murine models of DS, we found that OCNs restored osteoclast differentiation. This new action suggests potential facile translation into the clinic for conditions involving excess H2S exemplified by DS.

Keywords

Humans, Animals, Mice, Hydrogen Sulfide, Thiosulfates, Carbon, Down Syndrome, Sulfides, Oxidation-Reduction, Polyethylene Glycols, nanozyme, hydrogen sulfide, catalysis, translational research

Published Open-Access

yes

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