2. Oxidative stress

Free radicals are species (molecules, ions) that contain free electrons (unpaired) in their structure and, as such, are usually highly reactive with other molecules [1]. Due to this reactivity, radicals can damage membranes and other cellular structures under oxidative stress conditions.

Oxidation reactions cause the formation of a variety of unstable reactive species that can trigger chain reactions in milliseconds, leading to disease and programmed cell death (apoptosis) [2]. Among the reactive species formed are reactive oxygen species (ROS), which participate in several physiological and pathological processes in the organism.

With the evolution of the cell and the use of molecular oxygen in energy metabolism, ROS began to play increasingly studied and significant roles in a number of diseases [3]. The main ROS are the superoxide anion radical (O2 ), hydrogen peroxide (H2O2), and the hydroxyl radical (OH), the last being the most reactive and harmful [1].

Given that free radical production occurs naturally in the organism, an elaborate endogenous antioxidant system evolved to control the harmful effect of reactive species. This system includes antioxidant scavenger enzymes such as superoxide-dismutase (SOD) 1 and 2, catalase, glutathione (GSH), and related enzymes, including glutathione peroxidase (GPx), glutathione S-transferase (GST), and glutathione reductase (GSH-Red), which converts ROS into neutral, non-reactive molecules.

Thus, hearing losses with different etiologies have been studied at the cellular and molecular level, and there is a convergent tendency with respect to the association between them and oxidative stress.
