Abstract
Redox stress is a significant contributor to the molecular dysfunction associated with traumatic brain injury (TBI). Each of the canonical molecular biomarkers of TBI, including GFAP and UCHL1, demonstrate a clear relationship with redox stress via protein oxidation and enzymatic inhibition. Additionally, several markers of redox stress have demonstrated utility in assessing preclinical and clinical TBI, including F2-isoprostanes, generated from the oxidation of arachidonic acid. Thus, we investigated the role of urinary 8-isoprostane as a biomarker for delineating between sham and impacted mice. In this study, male and female mice (n = 19) subjected to five daily impacts using a repeated impact acceleration (rIA) model were evaluated against sham mice for neurological deficits. Impacted mice exhibited behavioral deficits, with increases in righting reflex (RR) times (p 2 = 0.75; p 2 = 0.08; p > 0.05). Overall, these results suggest repeated impacts using a preclinical TBI mouse model induce acute neurobehavioral deficits, assessed via RR and mNSS, and molecular deficits, including increases in GFAP and urinary 8-isoprostane.