• Leonardo Lorente, María M Martín, Agustín F González-Rivero, Antonia Pérez-Cejas, Pedro Abreu-González, Luis Ramos, Mónica Argueso, Juan J Cáceres, Jordi Solé-Violán, Andrea Alvarez-Castillo, Alejandro Jiménez, and Victor García-Marín.
• Intensive Care Unit, Hospital Universitario de Canarias, Ofra, s/n. La Laguna, 38320, Santa Cruz de Tenerife, Spain. lorentemartin@msn.com.
• Neurocrit Care. 2020 Jun 1; 32 (3): 790-795.

BackgroundThe hyperoxidative state in traumatic brain injury (TBI) could produce oxidative damage on the ribonucleic acid (RNA) and deoxyribonucleic acid (DNA). Oxidative damage to nucleic acids in TBI patients has been studied, and higher concentrations of 8-OHdG were found in postmortem brain samples of subjects who died following TBI than in subjects who died from sudden cardiac death. Thus, the objective of this study was to determine whether there is an association between serum DNA and RNA oxidative damage and mortality in TBI patients.MethodsWe included patients with severe isolated TBI defined as a lower score than 9 points in the Glasgow Coma Scale (GCS) and lower than 9 points in non-cranial aspects in the Injury Severity Score. We determined serum concentrations of the three oxidized guanine species (OGS) (8-OHdG from DNA, 8-hydroxyguanosine from RNA, and 8-hydroxyguanine from DNA or RNA) and malondialdehyde (to estimate lipid peroxidation) on the day of TBI. Mortality at 30 days was the end-point study.ResultsWe found higher serum concentrations of OGS (p < 0.001) and malondialdehyde (p < 0.001) in non-surviving (n = 34) than in surviving patients (n = 90), an association between serum OGS levels and 30-day mortality after control for CGS, age, and computed tomography findings (OR = 1.397; 95% CI = 1.137-1.716; p = 0.001), and a positive correlation between serum levels of OGS and malondialdehyde (rho = 0.24; p = 0.01).ConclusionsTo our knowledge, our study is the largest series reporting data on DNA oxidative damage in TBI patients and is the first reporting DNA and RNA oxidative damage in TBI patients associating lipid peroxidation and mortality.

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