Related Experiment Video
Updated: May 19, 2026

High-Resolution Fluoro-Respirometry of Equine Skeletal Muscle
Published on: February 3, 2023
Mechanisms of oxidative injury in equine disease
David M Wong1, Rustin M Moore, Charles W Brockus
1Iowa State University, Ames, IA, USA.
Abstract:
Oxygen is essential to aerobic life, but it is also associated with the production of highly reactive compounds that can pose danger to physiologic systems when the oxygen concentration is excessive. Reactive oxygen species (ROS) are required for normal physiologic processes, but when produced in excess, they can overwhelm endogenous antioxidants, resulting in significant cellular damage and, eventually, cell death. Ischemic events can initiate numerous pathophysiologic mechanisms leading to increased production of ROS, loss of cellular energy production, and lipid peroxidation. Although reperfusion is a necessary step in cellular recovery from ischemia, it can be deleterious by leading to the generation of even more ROS and stimulating the accumulation of neutrophils. Both of these processes may contribute to irreversible cell death and, ultimately, organ failure. This article reviews oxygen metabolism, ischemia, and reperfusion injury and how these processes may occur in equine disorders.
Related Concept Videos
Cellular Injury I: Introduction
Oxidation of Phenols to Quinones
o-hydroxy phenols are oxidized to o-quinones and p-hydroxy phenols to p-quinones. Such redox reactions involve the transfer of two electrons and two protons. The reversible redox property is crucial in...
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Peroxisomes
Electron Transport Chain: Complex III and IV
The Electron Transport Chain
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...

