J Surg Res. 2025 Dec 3;317:27-37. doi: 10.1016/j.jss.2025.11.008. Online ahead of print.
ABSTRACT
INTRODUCTION: Hydrogen sulfide (H2S) is a ubiquitous gas that has recently garnered significant interest as a potential therapeutic agent for various ischemic and inflammatory diseases. Therefore, effective H2S detection methods may be beneficial for translational research applications for these diseases. In the current study, a near-infrared H2S (NIR-HS) probe was synthesized and hypothesized that the probe would allow for qualitative assessment of H2S in biological systems.
MATERIALS AND METHODS: The NIR-HS probe was synthesized and purified using chromatography. The ability of the NIR-HS probe to detect H2S was first determined in cell-free environments when H2S salts sodium sulfide (Na2S), sodium hydrosulfide (NaHS) and a H2S-slow-releasing donor (p-methoxyphenyl)morpholino-phosphinodithioic acid (GYY4137), were used. Three mammalian cell lines (HIEC6, HEK293T, and vertebral bone adherent mesenchymal stem cell) were treated with NaHS (H2S donor) or ZnCl2 (negative control) in the presence of the NIR-HS probe. NIR-HS probe was also tested in cells that either overexpressed H2S synthases (CBS, CTH, and mercaptopyruvate sulfurtransferase) or had reduced levels of H2S synthases. The fluorescent responses of NIR-HS were determined by fluorescent microscopy and flow cytometry.
RESULTS: In a cell-free system, the NIR-HS probe showed a statistically significant increase in fluorescence with the addition of Na2S, NaHS, or GYY4134 compared to vehicle alone, and dose-dependent responses to H2S donors. In mammalian cells, H2S donors increased and ZnCl2 decreased the fluorescent responses of NIR-HS. Knocking down and overexpressing the endogenous H2S synthases altered the production of H2S, respectively.
CONCLUSIONS: This NIR-HS probe was shown to be a useful compound in the detection of H2S in cell-free and cellular environments. Further studies are needed to demonstrate its use within in vivo applications of specific ischemic and inflammatory disease models prior to clinical translation.
PMID:41343914 | DOI:10.1016/j.jss.2025.11.008
