Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling

Publication date: Available online 22 August 2018Source: Molecular Aspects of MedicineAuthor(s): Albert van der Vliet, Yvonne M.W. Janssen-Heininger, Vikas AnathyAbstractThe lung is a delicate organ with a large surface area that is continuously exposed to the external environment, and is therefore highly vulnerable to exogenous sources of oxidative stress. In addition, each of its approximately 40 cell types can also generate reactive oxygen species (ROS), as byproducts of cellular metabolism and in a more regulated manner by NOX enzymes with functions in host defense, immune regulation, and cell proliferation or differentiation. To effectively regulate the biological actions of exogenous and endogenous ROS, various enzymatic and non-enzymatic antioxidant defense systems are present in all lung cell types to provide adequate protection against their injurious effects and to allow for appropriate ROS-mediated biological signaling. Acute and chronic lung diseases are commonly thought to be associated with increased oxidative stress, evidenced by altered cellular or extracellular redox status, increased irreversible oxidative modifications in proteins or DNA, mitochondrial dysfunction, and altered expression or activity of NOX enzymes and antioxidant enzyme systems. However, supplementation strategies with generic antioxidants have been minimally successful in prevention or treatment of lung disease, most likely due to their inability to distinguish between harmful and benefici...
Source: Molecular Aspects of Medicine - Category: Molecular Biology Source Type: research