The impact of and changes in the oxidative status in the post-injury period following nonpenetrating traumatic brain injuries

ObjectiveIn the pathogenesis of the post-injury period following nonpenetrating traumatic brain injuries (TBIs; post-TBIs), pathological metabolic changes in the oxidative status are important, as a complete understanding of their interactions can explain the concept of how oxidative metabolic-related differences develop, thereby supporting effective treatment.MethodsThis case-control study included 63 patients (mean age ± SD, 36.19 ± 11.4 years) in the post-TBI group and 32 healthy controls. Participants were tested for creatine kinase, adenosine triphosphate, and adenosine diphosphate levels using enzyme-linked immunosorbent assays and for pyruvate and lactate levels using a spectrophotometric method according to standard manufacturer protocols.ResultsThis study found abnormally decreased adenosine triphosphate and adenosine diphosphate levels in the general nonpenetrating post-TBI group versus controls. The median total adenosine triphosphate levels were 600.4 ± 46.96 in the general clinical group and 745.7 ± 49.83 mkmol/L in controls (p < 0.0001, t = 13.69, 95% confidence interval: 124.0 to 166.5). The median total adenosine diphosphate levels were 247.6 ± 33.09 in the general clinical group and 273.9 ±31.98 mkmol/L in controls (p = 0.0004, t = 3.734, 95% confidence interval: 12.20 to 40.26). Compared with controls, elevated creatine kinase levels were found in the general clinical group (p < 0.0001, t = 7.030, 95% confidence interval: -39.78 to -22.19). The median total creatine kinase (mean ± SD) levels were 129.6 ± 21.37 in the general clinical group and 98.61 ± 19.74 IU/L in controls. Higher creatine kinase (p < 0.0001, t = 4.779, 95% confidence interval: 13.16 to 32.23) and lower adenosine triphosphate levels (p < 0.001, t = 4.997, 95% confidence interval: -70.74 to -30.31) were found to be more pronounced after brain contusion compared with those following mild TBIs.ConclusionsNonpenetrating post-TBIs showed higher creatine kinase levels associated with lower adenosine triphosphate-adenosine diphosphate levels, indicating oxidative dyshomeostasis at 12-month post-injury follow-ups, which could play a pathogenetic role in post-TBIs progression.