Oxidation of Hydrogen Sulfide to Polysulfide and Thiosulfate by a Carbon Nanozyme: Therapeutic Implications with an Emphasis on Down Syndrome.
basic_science · Level V
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- Record sourced from PubMed, PMID 37272655.
- Also identified by DOI 10.1002/adma.202211241 and PMC identifier 10696138.
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Abstract
Hydrogen sulfide (H<sub>2</sub> S) is a noxious, potentially poisonous, but necessary gas produced from sulfur metabolism in humans. In Down Syndrome (DS), the production of H<sub>2</sub> S is elevated and associated with degraded mitochondrial function. Therefore, removing H<sub>2</sub> S from the body as a stable oxide could be an approach to reducing the deleterious effects of H<sub>2</sub> S in DS. In this report we describe the catalytic oxidation of hydrogen sulfide (H<sub>2</sub> S) to polysulfides (HS<sub>2+n</sub> <sup>-</sup> ) and thiosulfate (S<sub>2</sub> O<sub>3</sub> <sup>2-</sup> ) 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 H<sub>2</sub> S to polysulfides and S<sub>2</sub> O<sub>3</sub> <sup>2-</sup> in a dose-dependent manner. The reaction is dependent on O<sub>2</sub> 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 H<sub>2</sub> S 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 H<sub>2</sub> S exemplified by DS.
Medical subject headings
- Hydrogen Sulfide
- Down Syndrome