Biochemical Mechanisms of Oxidative Stress and Antioxidant Defense Systems in Disease Progression: A Review

Oxidative stress is a basic biochemical disturbance resulting from an imbalance and overproduction of reactive oxygen and nitrogen species when the level exceeds the cellular antioxidant capacity. We need controlled reactive species for signaling, immune defense, mitochondrial adaptation and vascular control; yet persistent imbalance in redox equilibrium favors lipid peroxidation, protein oxidation, DNA damage, mitochondrial dysfunction and inflammation which results in progressive tissue damage. Traditionally, the concept of antioxidant defense has been restricted to isolated pathways, but lately it has been emphasized that such mechanisms are coordinated and comprise enzymes (superoxide dismutase, catalase, glutathione peroxidase, peroxiredoxins and thioredoxin systems) in conjunction with nonenzymatic antioxidants (glutathione, vitamins C and E, carotenoids, melatonin. uric acid, selenium-containing molecules, from selenium enriched foods—and dietary polyphenols). Oxidative stress and its contribution to the pathology of cardiovascular disease, diabetes mellitus, carcinogenesis, neurodegenerative disorders, chronic kidney injury with fibrosis in development related liver injury as well as inflammatory bowel disease are highlighted Processes associated with aging-related degeneration Sources of oxidative damage. In this review, we discuss the biochemical origins of reactive species, a multitiered antioxidant protection system, primary redox biomarkers, and disease pathways. Finally, it highlights the need for caution in interpretation of antioxidant therapy as nonstaged or over-supplemented and/or uncontrolled pathways to the disease state may fail where authorities exist.