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Oxidative Stress in Traumatic Brain Injury

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Traumatic brain injury (TBI) is a major healthcare concern, constituting a major cause of death and disability throughout the world. Among the factors leading to TBI outcome are biochemical cascades which occur in response to primary and secondary injury. These mechanisms generate oxidative stress, an imbalance between oxidant and antioxidant agents that can result in neural dysfunction and death. After TBI, an assembly of oxidative stress markers (carbonylated proteins, lipid peroxides, reactive oxygen and reactive nitrogen species) are produced in the brain, while antioxidant defense enzymes decrease (GSH, ratio GSH/GSSG, GPx, GR, GST, G-6PD, SOD, CAT). This imbalance is directly related to the pathogenesis of TBI. Therefore, the development of antioxidant strategies is of primary interest in ongoing efforts to optimize brain injury treatment. The success of any drug intervention strategy relies, in part, on knowledge of the optimal dosage and therapeutic window for its administration. But while the enzymes involved in oxidative stress have been identified, the temporal course of this imbalance following TBI has yet to be determined. This would explain why most antioxidant strategies developed to treat patients with TBI have failed.

Keywords: Brain damage; cerebral ischemia; oxidative stress biomarker; reactive oxygen species; traumatic brain injury

Document Type: Research Article

Publication date: April 1, 2014

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.

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