: Stroke is the second leading cause of mortality and the major cause of adult physical disability worldwide. The current available treatment to recanalize the blood flow in acute ischemic stroke is intravenous administration of tissue plasminogen activator (t-PA) and endovascular treatment. Nevertheless, those treatments have the disadvantage that reperfusion leads to a highly harmful reactive oxygen species (ROS) production, generating oxidative stress (OS), which is responsible for most of the ischemia-reperfusion injury and thus causing brain tissue damage. Also, OS can lead brain cells to apoptosis, autophagy and necrosis. The aims of this review are to provide an updated overview of the role of OS in brain IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI after stroke.

Renal transplant (RT) is the definitive treatment for end-stage renal disease, which is known as a high prevalence pathology with strong economic repercussion both for patients and health systems. Solid organ transplantation is a classically described clinical setting in which massive amounts of reactive oxygen species (ROS) are produced due to ischaemia-reperfusion, thus becoming an essential pathophysiological element involved in delayed graft function in the context of RT. Nevertheless, no clinical protocol yet exists to counteract the damage mediated by ROS intensively produced throughout the transplant process. The available evidence shows a number of successful experiences in the use of antioxidant supplementation and reinforcement over other oxidative stress-related pathologies. This article addresses the pathophysiological role of oxidative stress in RT and its known consequences in function and structure of the allograft, with the objective of gathering consistent information that demonstrates the central role of oxidative stress in this pathology, and to consider it as a possible therapeutic approach in the future.