As an outcome, the interaction of superoxide anion with NO generates peroxynitrite (ONOO−), and the excessive generation of ONOO− triggers nitrative stress.
Here, from our review of the literature, we suggest that increases in circulating LPS and an excessive generation of ROS are the main actors in the acute inflammatory process generated by excessive AE.
Pathogenesis is multifactorial and includes excessive generation of reactive oxygen species that interact with and consume nitric oxide (NO), generating peroxynitrite and resulting in oxidation of tetrahydrobiopterin and promotion of NO uncoupling.
Low physiological levels of ROS are generated in the muscles to maintain the normal tone and contractility, but excessive generation of ROS promotes contractile dysfunction resulting in muscle weakness and fatigue [ 29].
Excessive generation of free radicals is regarded as a major detrimental factor in cerebral ischemic insults.
Alterations in mitochondrial membrane potential lead to neuronal death by excessive generation of free radicals, inflammatory cytokines, and excitotoxins.
Oxidative stress, resulting from excessive generation of reactive oxygen species (ROS), plays a pivotal role in the initiation and progression of inflammatory bowel disease (IBD).
Nowadays, the raise of excessive generation of solid wastes is considered as a major environmental concern due to the fast global population growth.
Oxidative stress resulting in excessive generation of ROS is a compelling initiator of DNA damage along with damage to various cellular proteins and other macromolecules.
In conclusion, our data suggest that EC-SOD plays an important role in the protection from skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.
There is considerable evidence that during Salmonella-induced infection, excessive generation of reactive oxygen species (ROS), like inflammatory molecules occurs which results into lipid peroxidation thereby causing damage to the host cell (Pacher et al. 2007).
