Mechanism of H 2 S-mediated protection against oxidative stress in Escherichia coli

Significance Hydrogen sulfide (H 2 S) is a highly toxic gas that interferes with cellular respiration; however, at low physiological amounts, it plays an important role in cell signaling. Remarkably, in bacteria, endogenously produced H 2 S has been recently recognized as a general protective molecule, which renders multiple bacterial species highly resistant to oxidative stress and various classes of antibiotics. The mechanism of this phenomenon remains poorly understood. In this paper, we use Escherichia coli as a model system to elucidate its major enzymatic source of H 2 S and establish the principle biochemical pathways that account for H 2 S-mediated protection against reactive oxygen species. Understanding those mechanisms has far-reaching implications in preventing bacterial resistance and designing effective antimicrobial therapies.