Characterization of hydrogen sulfide toxicity to human corneal stromal fibroblasts

Abstract

Abstract Hydrogen sulfide gas (H 2 S) is a chemical weapon and a common environmental pollutant. H 2 S intoxication is lethal to humans and animals. H 2 S contact to the eye can cause vision loss. However, the molecular mechanisms associated with H 2 S toxicity to the cornea remain unclear, and no specific therapy exists to mitigate ocular damage from H 2 S. Here, we report H 2 S‐induced cytotoxicity and the parameters contributing to the molecular mechanisms associated with corneal toxicity using primary human corneal stromal fibroblasts (hCSFs) in vitro . Sodium hydrosulfide (NaSH) was used as a source of H 2 S, and the cytotoxicity of H 2 S was determined by treating hCSF cells with varying concentrations of NaSH (0–10 mM) for 0–72 hours. Changes in cell proliferation, oxidative stress factors, and the expression of inflammatory and fibrotic genes were studied using standard commercial kits and qRT‐PCR. NaSH exposure to hCSFs showed dose‐ and time‐dependent cytotoxicity. The IC 50 of NaSH was determined to be 5.35 mM. NaSH 5.35 mM exposure led to significantly decreased cytochrome c oxidase activity, increased ROS production, and increased expression of inflammatory and fibrotic genes in hCSF cells. H 2 S/NaSH exposure alters normal mitochondrial function, oxidative stress, and inflammatory and fibrotic gene responses in corneal stromal fibroblasts in vitro .