| Abstract |
The highly reactive superoxide radicals forms when dioxides interact with air, a process that can be achieved in all living organisms and can then be further purposed depending on its context and the process through which it is metabolized. This reaction can occur endogenously through various metabolic pathways and can result in the formation of different reactive oxygen species (ROS), such as hydrogen peroxide (HO), hypochlorite (ClO), peroxynitrite (ONOO), and hydroxyl radical (OH). Historically considered dangerous, free radicals were given the responsibility as the perpetrators of numerous pathophysiological states, such as cardiovascular disease, inflammation, hereditary diseases, aging, and many other diseases. Even though it is known that these diseases thrive under the overproduction of free radicals, superoxides also have a pivotal role in maintaining physiological states. These include defense functions like antibacterial properties and phagocytosis, as well as their ability to act as signaling molecules. Superoxides are also included as part of the process of cell death and cellular disfunction, given their ability to react with distinct biomolecules, such as proteins, lipids, and DNA. These superoxide molecules can be produced in various cell sites, including the cytosol, endoplasmic reticulum, peroxisomes, and mitochondria, the latter generating and compartmentalizing almost 90% of the reactive oxygen species, mainly through coenzyme Q. Given its active part in many of the body's reactions, intricate regulation is achieved by the enzyme superoxide dismutases (SODs), which catalyzes the deactivation of superoxide and maintains the physiological concentration of superoxides. Due to the complexity and importance of superoxide radicals in various metabolic processes, they play a role in various diseases, including inflammation-driven diseases, atherosclerosis, cancer, and other pathologies that pose a burden to modern-day society. Copyright © 2024, StatPearls Publishing LLC. |
