Oxidative stress is defined as an excessive load of reactive oxygen species (ROS), which cause ongoing or reversible damage in the body. This can occur in individual cells, and in specific body organs, and can affect the health of patients at the whole body level.
Antioxidants can chemically react with ROS to quench and thus inactivate these reactive, damaging molecules. Cystic fibrosis is characterized by oxidative stress throughout the body and chronic inflammation in the lungs. Patients with CF are deficient in the body’s major anti-oxidant, glutathione (GSH). This is thought to be due to many reasons, including dietary insufficiency, but being the major anti-oxidant of the body, GSH is highly utilized in areas of oxidative stress and inflammation. GSH serves multiple functions and is utilized by cells to regulate physiological functions such as DNA transcription, RNA translation, and subsequent protein synthesis. It is utilized to regulate protein functions and is vital in regulating dietary absorption of nutrients, storage and availability of essential proteins and fatty acids.
Oxidation reactions are essential to fight infection and are generated when neutrophils ingest bacteria to rid the body of pathogens. For reasons still unclear, in CF, the environment in the airways is strongly pro-inflammatory. After neutrophils have been recruited, neutrophil-derived oxidants are released into the airways, and contribute to ongoing tissue destruction. Oxidants, which include hydrogen peroxide, hypochlorous acid, and other damaging particles called free radicals are released and create a vicious perpetual cycle of tissue destruction.