Reactive oxygen species (ROS) are formed when electrons react with oxygen, leading to their transformation into highly reactive molecules. While ROS can cause significant damage to proteins, lipids, and nucleic acids, they also play crucial roles in various physiological processes and diseases. Low to moderate concentrations of ROS regulate cell signaling cascades, while high concentrations can lead to non-specific damage. ROS are produced by multiple sources, including NADPH oxidase enzymes, and are degraded by various systems. Their roles in health include redox regulation of protein phosphorylation, ion channels, and transcription factors, as well as biosynthetic processes like thyroid hormone production and extracellular matrix crosslinking. ROS-related diseases can result from either insufficient or excessive ROS levels. Antioxidant supplementation has shown limited effectiveness in clinical studies, likely due to its late action and non-specificity. Specific inhibition of ROS-producing enzymes, such as NADPH oxidases, shows more promise for clinical efficacy. The article discusses the sources, mechanisms, and roles of ROS in health and disease, emphasizing the importance of understanding their balance for therapeutic interventions.Reactive oxygen species (ROS) are formed when electrons react with oxygen, leading to their transformation into highly reactive molecules. While ROS can cause significant damage to proteins, lipids, and nucleic acids, they also play crucial roles in various physiological processes and diseases. Low to moderate concentrations of ROS regulate cell signaling cascades, while high concentrations can lead to non-specific damage. ROS are produced by multiple sources, including NADPH oxidase enzymes, and are degraded by various systems. Their roles in health include redox regulation of protein phosphorylation, ion channels, and transcription factors, as well as biosynthetic processes like thyroid hormone production and extracellular matrix crosslinking. ROS-related diseases can result from either insufficient or excessive ROS levels. Antioxidant supplementation has shown limited effectiveness in clinical studies, likely due to its late action and non-specificity. Specific inhibition of ROS-producing enzymes, such as NADPH oxidases, shows more promise for clinical efficacy. The article discusses the sources, mechanisms, and roles of ROS in health and disease, emphasizing the importance of understanding their balance for therapeutic interventions.