Abstract
Extracellular superoxide dismutase (EcSOD) is the only extracellular scavenger of superoxide anion (O2.-) with unique binding capacity to cell surface and extracellular matrix through its heparin-binding domain. Enhanced EcSOD activity prevents oxidative stress and damage, which are fundamental in a variety of disease pathologies. In this review we will discuss the findings in humans and animal studies supporting the benefits of EcSOD induced by exercise training in reducing oxidative stress in various tissues. In particularly, we will highlight the importance of skeletal muscle EcSOD, which is induced by endurance exercise and redistributed through the circulation to the peripheral tissues, as a molecular transducer of exercise training to confer protection against oxidative stress and damage in various disease conditions. …
1. Introduction
Oxygen is indispensable for life; however, under certain situations it has deleterious effects due to the formation and activity of a number of chemical compounds, known as free radicals or reactive oxygen species (ROS) [46]. Fortunately, cellular enzymatic and nonenzymatic mechanisms are in place to neutralize ROS. Among the members of the enzymatic defense system, superoxide dismutases (SODs) are an ubiquitous family of enzymes that catalyze the dismutation of superoxide anions (O2.-) as the first line of defense against ROS [117]. SODs reduce O2.- to oxygen and hydrogen peroxide (H2O2), and H2O2 is further neutralized to water through enzymatic reactions by catalase (CAT) or glutathione peroxidase (GPX). These reactions are necessary to maintain redox balance. However, excessive ROS production can exceed the capacity of the antioxidant defense system leading to oxidative stress, which causes cellular damage by oxidizing proteins, lipids, DNA/RNA, and other macromolecules. Oxidative stress has been shown to play an important role in many disease pathologies, such as cachexia, sepsis, hypertension, myocardial infarction (MI), chronic heart failure (CHF), chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS) [31,35]. There are three SOD isoenzymes; each resides in a distinct cellular location SOD1, or CuZnSOD, is a copper and zinc-containing homodimer in cytoplasm. SOD2, or MnSOD, exists as a tetrameric manganese-containing enzyme in the matrix of mitochondria. SOD3, or EC-SOD, is a copper and zinc-containing tetrameric enzyme that is secreted from the producing cells into the extracellular space [117]…
To read the entire article from Science Direct, click https://www.sciencedirect.com/science/article/pii/S2213231720303190?via%3Dihub