During secondary pathophysiological cascades of early brain injury (EBI) after traumatic brain injury (TBI), reactive oxygen species (ROS) act rapidly play a pivotal role in the pathogenesis, neurodegeneration and prognosis of EBI via damaging lipid, protein and nucleic acid. However, the time spot of biological sample collection of oxidation-stress in TBI animal model lag behind in clinical observation or in theoretical datum. This paradox and the related methodology are reviewed in this paper.
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| http://dx.doi.org/10.11817/j.issn.1672-7347.2014.02.015 | DOI Listing |
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