Reactive Oxygen Species ROS

What reactive oxygen species are

Reactive oxygen species (ROS) are chemically reactive oxygen-containing molecules that include free radicals, such as superoxide, and non-radical oxidants, such as hydrogen peroxide.^[1] ROS are continuously generated in human tissues as a normal by-product of aerobic metabolism and as part of immune defense.^[2] At physiological levels, ROS act as signaling molecules that regulate cell growth, barrier repair, and immune responses.^[3] When ROS production exceeds antioxidant control, oxidative stress develops, which disrupts normal redox signaling and can damage proteins, lipids, and DNA.^[4]

Major biological sources of ROS in the gut

In the gastrointestinal tract, ROS arise from multiple sources, including mitochondria, activated neutrophils, macrophages, and epithelial NADPH oxidase enzymes.^[5] NADPH oxidases (NOX and DUOX families) are unique in that they exist primarily to generate ROS for host defense and cell signaling, rather than as accidental metabolic by-products.^[6] In the gut epithelium, NOX1- and DUOX-derived ROS contribute to barrier homeostasis and antimicrobial defense at the mucosal surface.^[7]

ROS as a mediator of host–microbiome interactions

ROS are central to how the host shapes the microbiome and responds to microbes. Epithelial ROS can restrict pathogen growth and influence microbial colonization patterns by creating localized oxidative conditions at the mucosal surface.^[8] In a mechanistic mouse study, loss of epithelial NADPH oxidase activity reshaped the gut microbiota. It unexpectedly promoted a compensatory enrichment of hydrogen peroxide–producing commensals that reduced pathogen virulence, illustrating a three-way relationship between host ROS, microbiota adaptation, and infection outcomes.^[9] This evidence supports ROS as a microbiome-relevant “host ecology signal,” not simply a marker of damage.^[10][11]

However, excessive ROS can also contribute to inflammation and barrier dysfunction. In intestinal inflammation, increased oxidant generation can destabilize tight junction regulation and promote epithelial injury, which increases mucosal exposure to microbial products and can amplify immune activation.^[12][13] This creates a clinically important feedback loop in which inflammation increases ROS, and ROS can further worsen barrier integrity and inflammatory signaling.^[14][15]

Clinical interpretation in microbiome medicine

In microbiome medicine, ROS-related biology is relevant in inflammatory bowel disease, enteric infection, metabolic inflammation, and conditions associated with barrier impairment.^[16][17] Clinically, ROS are not measured as a single “ROS test,” because ROS are short-lived and vary by location and chemistry.^[18] Consensus guidance emphasizes that accurate assessment requires measuring specific ROS species or validated downstream oxidative damage products rather than relying on nonspecific probes.^[19] For patient care, the most practical approach is integrating inflammation markers, barrier evaluation, and microbiome patterns to infer ROS-driven pathology when clinically supported.^[20][21]

Research Feed

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