The article explores the intricate relationship between the intestinal flora, the kynurenine pathway, and mitochondrial oxidative stress. The gut microbiota, or intestinal flora, plays a crucial role in influencing brain development and function through the metabolism of tryptophan (Trp) into various metabolites, including kynurenic acid (KYNA) and quinolinic acid (QUIN). These metabolites can affect neuronal excitotoxicity and mitochondrial function, contributing to conditions such as depression, schizophrenia, and migraine. The kynurenine pathway is particularly important in maintaining redox balance and energy production in mitochondria. Mitochondrial disorders, which are often challenging to diagnose and treat, are linked to disruptions in this pathway, leading to oxidative stress and cellular damage. The article highlights the potential therapeutic targets for managing mitochondrial disorders by modulating the gut microbiota and the kynurenine pathway. Additionally, it discusses the role of specific metabolites, such as KYNA and QUIN, in the pathophysiology of mitochondrial diseases and their potential as biomarkers. The review emphasizes the need for further research to understand the complex interactions between the gut microbiota, the kynurenine pathway, and mitochondrial function, and to develop effective therapeutic strategies.The article explores the intricate relationship between the intestinal flora, the kynurenine pathway, and mitochondrial oxidative stress. The gut microbiota, or intestinal flora, plays a crucial role in influencing brain development and function through the metabolism of tryptophan (Trp) into various metabolites, including kynurenic acid (KYNA) and quinolinic acid (QUIN). These metabolites can affect neuronal excitotoxicity and mitochondrial function, contributing to conditions such as depression, schizophrenia, and migraine. The kynurenine pathway is particularly important in maintaining redox balance and energy production in mitochondria. Mitochondrial disorders, which are often challenging to diagnose and treat, are linked to disruptions in this pathway, leading to oxidative stress and cellular damage. The article highlights the potential therapeutic targets for managing mitochondrial disorders by modulating the gut microbiota and the kynurenine pathway. Additionally, it discusses the role of specific metabolites, such as KYNA and QUIN, in the pathophysiology of mitochondrial diseases and their potential as biomarkers. The review emphasizes the need for further research to understand the complex interactions between the gut microbiota, the kynurenine pathway, and mitochondrial function, and to develop effective therapeutic strategies.