The role of gut microbiota in intestinal disease: from an oxidative stress perspective Recent studies have shown that gut microbiota-mediated oxidative stress is significantly associated with intestinal diseases such as colorectal cancer, ulcerative colitis, and Crohn's disease. The level of reactive oxygen species (ROS) increases when the gut microbiota is dysregulated, especially when several gut bacterial metabolites are present. Although healthy gut microbiota plays a vital role in defending against excessive oxidative stress, intestinal disease is significantly influenced by excessive ROS, and this process is controlled by gut microbiota-mediated immunological responses, DNA damage, and intestinal inflammation. This review discusses the relationship between gut microbiota and intestinal disease from an oxidative stress perspective and provides a summary of the most recent therapeutic approaches for preventing or treating intestinal diseases by modifying gut microbiota. Oxidative stress, characterized by an imbalance between the generation and elimination of ROS, not only occurs in the inflamed intestinal mucosa but also extends into the deeper layers of the intestinal wall. The gut microbiota can modulate cellular ROS concentrations. Lactobacillus and Bifidobacterium in the gastrointestinal tract can enzymatically convert nitrate and nitrites into nitric oxide (NO), which provides the gut epithelia with a substantial reservoir of NO. Similarly, the production of NO can be observed in Streptococcus and bacillus through the utilization of L-arginine. In the context of nanomolar concentrations, NO is commonly recognized as having a protective effect. At higher concentrations, it elicits deleterious effects through the production of ROS, including superoxide (O₂⁻) and hydrogen peroxide (H₂O₂), which subsequently give rise to highly reactive hydroxyl radicals. This process has been implicated in the pathogenesis of IBD and CRC. The reduction in ROS is facilitated by the influence of gut bacteria-generated beneficial metabolites, specifically short-chain fatty acids (SCFAs), which are considered metabolic byproducts produced by certain bacterial species. These SCFAs can serve as an energy source for other bacterial species through a phenomenon referred to as cross-feeding. Furthermore, SCFAs can directly modify the cells of the host's intestinal tract. For example, butyrate, a prominent SCFA, is widely recognized for its role as a major energy provider for colonocytes and its contribution to the restoration of intestinal epithelial cells. The dysbiosis of gut microbiota has been found to be associated with the generation of ROS, which specifically interact with cysteine redox switches present in proteins. This phenomenon induces modifications in immune responses, resulting in DNA impairment and provoking inflammation within the gastrointestinal tract. The precise mechanisms by which bacteria may influence the progression of disease remain incompletely understood, despite the identification of certain members of the gut microbiota that have been implicated as causative agents in intestinal disorders. The crosstalk between gut microbiota and oxidative stress is bidirectional. TheThe role of gut microbiota in intestinal disease: from an oxidative stress perspective Recent studies have shown that gut microbiota-mediated oxidative stress is significantly associated with intestinal diseases such as colorectal cancer, ulcerative colitis, and Crohn's disease. The level of reactive oxygen species (ROS) increases when the gut microbiota is dysregulated, especially when several gut bacterial metabolites are present. Although healthy gut microbiota plays a vital role in defending against excessive oxidative stress, intestinal disease is significantly influenced by excessive ROS, and this process is controlled by gut microbiota-mediated immunological responses, DNA damage, and intestinal inflammation. This review discusses the relationship between gut microbiota and intestinal disease from an oxidative stress perspective and provides a summary of the most recent therapeutic approaches for preventing or treating intestinal diseases by modifying gut microbiota. Oxidative stress, characterized by an imbalance between the generation and elimination of ROS, not only occurs in the inflamed intestinal mucosa but also extends into the deeper layers of the intestinal wall. The gut microbiota can modulate cellular ROS concentrations. Lactobacillus and Bifidobacterium in the gastrointestinal tract can enzymatically convert nitrate and nitrites into nitric oxide (NO), which provides the gut epithelia with a substantial reservoir of NO. Similarly, the production of NO can be observed in Streptococcus and bacillus through the utilization of L-arginine. In the context of nanomolar concentrations, NO is commonly recognized as having a protective effect. At higher concentrations, it elicits deleterious effects through the production of ROS, including superoxide (O₂⁻) and hydrogen peroxide (H₂O₂), which subsequently give rise to highly reactive hydroxyl radicals. This process has been implicated in the pathogenesis of IBD and CRC. The reduction in ROS is facilitated by the influence of gut bacteria-generated beneficial metabolites, specifically short-chain fatty acids (SCFAs), which are considered metabolic byproducts produced by certain bacterial species. These SCFAs can serve as an energy source for other bacterial species through a phenomenon referred to as cross-feeding. Furthermore, SCFAs can directly modify the cells of the host's intestinal tract. For example, butyrate, a prominent SCFA, is widely recognized for its role as a major energy provider for colonocytes and its contribution to the restoration of intestinal epithelial cells. The dysbiosis of gut microbiota has been found to be associated with the generation of ROS, which specifically interact with cysteine redox switches present in proteins. This phenomenon induces modifications in immune responses, resulting in DNA impairment and provoking inflammation within the gastrointestinal tract. The precise mechanisms by which bacteria may influence the progression of disease remain incompletely understood, despite the identification of certain members of the gut microbiota that have been implicated as causative agents in intestinal disorders. The crosstalk between gut microbiota and oxidative stress is bidirectional. The