Kong, YOlejar, KJOn, StephenChelikani, Venkata2020-08-042020-07-102020-072020-07-072076-3921MS2AW (isidoc)32664392 (pubmed)https://hdl.handle.net/10182/12307The gastrointestinal (GI) tract is crucial for food digestion and nutrient absorption in humans. However, the GI tract is usually challenged with oxidative stress that can be induced by various factors, such as exogenous pathogenic microorganisms and dietary alterations. As a part of gut microbiota, Lactobacillus spp. play an important role in modulating oxidative stress in cells and tissues, especially in the GI tract. Oxidative stress is linked with excessive reactive oxygen species (ROS) that can be formed by a few enzymes, such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs). The redox mechanisms of Lactobacillus spp. may contribute to the downregulation of these ROS‐forming enzymes. In addition, nuclear factor erythroid 2 (NFE2)‐related factor 2 (Nrf‐2) and nuclear factor kappa B (NF‐κB) are two common transcription factors, through which Lactobacillus spp. modulate oxidative stress as well. As oxidative stress is closely associated with inflammation and certain diseases, Lactobacillus spp. could potentially be applied for early treatment and amelioration of these diseases, either individually or together with prebiotics. However, further research is required for revealing their mechanisms of action as well as their extensive application in the future.16 pagesElectronicen© 2020 by the authors. Licensee MDPI, Basel, Switzerland.oxidative stressinflammationLactobacillus spp.gastrointestinal (GI) tractThe potential of Lactobacillus spp. for modulating oxidative stress in the gastrointestinal tractJournal Article10.3390/antiox9070610ANZSRC::06 Biological SciencesANZSRC::11 Medical and Health SciencesANZSRC::1101 Medical Biochemistry and MetabolomicsANZSRC::060107 Enzymes2076-3921ANZSRC::3101 Biochemistry and cell biologyANZSRC::3205 Medical biochemistry and metabolomicsANZSRC::3214 Pharmacology and pharmaceutical scienceshttps://creativecommons.org/licenses/by/4.0/Attribution