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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 370312, 10 pages
Review Article

Traumatic Brain Injury and NADPH Oxidase: A Deep Relationship

1Department for Life Quality Studies, Alma Mater Studiorum-University of Bologna, Augusto 237, 47921 Rimini, Italy
2Department of Pharmacy and Biotechnology, Alma Mater Studiorum-University of Bologna, Via Irnerio 48, 40126 Bologna, Italy
3Neurorehabilitation Unit, Emergency Department, AUSL of Bologna, Via B. Nigrisoli 2, 40133 Bologna, Italy

Received 15 January 2015; Accepted 18 March 2015

Academic Editor: Javier Egea

Copyright © 2015 Cristina Angeloni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.