Fig. 3.

A model of H₂S-mediated protection of E. coli cells from oxidative stress. The fraction of exogenous H₂O₂ in the cell periplasm reacts with cysteine to form cystine and water. This leads to a decrease in the intracellular cysteine content, followed by autoregulation shutdown of cysB gene and activation of CysB-regulated genes, including tcyP, which controls the transport of cystine from the periplasm to the cytoplasm. The increased flow of cystine/cysteine into the cell leads to an increase in the level of mstA-dependent generation of H₂S, which sequesters free iron, inhibits the Fenton reaction, and prevents the formation of the toxic hydroxyl radical [88].