Hydrogen sulfide inhalation induces changes in body physiology and lung gene expression in mice.

Hydrogen sulfide (H2S) inhalation injures the respiratory, immune, and nervous systems, altering homeostasis and health, but the molecular mechanisms have been still unclear. In this study, we tested the effects of different concentrations of H2S on immune index and enzyme activity of mouse tissues and measured differentially expressed genes (DEGs) in mouse lung tissues by transcriptome sequencing. The results showed that H2S significantly increased tumor necrosis factor-alpha (TNF-α) (p < 0.05), catalase (CAT) (p < 0.01) and glutathione peroxidase (GSH-Px) (p < 0.05) activity levels; 80 and 100 ppm H2S treatment significantly increased interleukin-1β(IL-1β), interleukin-10 (IL-10) (p < 0.01) and glutathione reductase activation coefficient (GRAC) (p < 0.01) but decreased malonaldehyde (MDA) and superoxide dismutase (SOD) levels (p < 0.05); 100 ppm H2S treatment significantly increased glutathione S-transferase (GST) and reactive oxygen species (ROS) levels (p < 0.01). In addition, 963 DEGs were identified in different group. These genes were notably involved in immune responses, DNA modification, enzymatic activity, and cell cycle processes. FGFBP1, GATA3, KLRG1 and TBX21 may be crucial roles in the response to H2S exposure. This study provides a reference and many differential genes for the study of hydrogen sulfide damage mechanism.