Mapping the oxidative landscape in cystic fibrosis: methodological frontiers and application.

Cystic Fibrosis (CF), a multi-organ disease stemming from CFTR gene mutations, is characterized by progressive pulmonary disease, chronic inflammation, and a pro-oxidative environment. The intricate relationship between CFTR dysfunction, oxidative stress, and inflammation underscores the need to accurately characterize oxidative stress markers to identify therapeutic targets. This review compiles and analyzes methodologies employed in the CF field for this purpose, presenting selected applications and outcomes while highlighting potential inconsistencies due to experimental variations. The review encompasses a wide array of analytical techniques. These include methods for direct reactive oxygen species (ROS) detection (e.g., superoxide, hydrogen peroxide), characterization of oxidative damage to lipids (e.g., TBARS, F2-isoprostanes; lipidomics), proteins (e.g., carbonylation, S-nitrosylation, S-glutathionylation; proteomics), and DNA (e.g., 8-OHdG). Assays for major non-enzymatic antioxidants (glutathione, vitamins), enzymatic antioxidant systems (superoxide dismutase, catalase, glutathione peroxidase), and total antioxidant capacity (TAC) are detailed. Furthermore, methods to assess mitochondrial function for studying oxidative stress in CF are discussed. The critical choice of experimental models (