Fig. 3
From: Gut microbes involvement in gastrointestinal cancers through redox regulation
Bacteria regulated redox reactions in gastrointestinal epithelial/cancer cells. Bacteria link to gastrointestinal epithelial/cancer cells through their receptors or secreting metabolites, affecting the release of ROS from gastrointestinal epithelial/cancer cells. The overproduction of ROS can lead to DNA single strand breaks, DNA double strand breaks, DNA recombination repair system damage, and DNA mutations. Excess ROS mainly act on the sulfhydryl (RSH) side chain of the active cysteine of the protein (metabolism-related enzyme). In response to ROS, the reduced sulfhydryl groups on cysteine deprotonate and are oxidized to form sulfenic acids (RSOH). Subsequently, sulfonic acid can react with o-sulfhydryl groups to form intramolecular or intermolecular disulfide bonds (RS-SR or RS-SR’) or bind to glutathionylation (RS-SG) of glutathione (GSH). Sulfonic acid can also be further oxidized to form sulfonic acids (RSO2H) or sulfonic acids (RSO3H). The modified protein usually loses activity or function. Excess ROS react directly with polyunsaturated fatty acids on the cell membrane, causing cell membrane protein damage and influencing signal receptors on the cell membrane and various downstream signaling pathways, including the EGFR, TNF, and Wnt signaling pathways