Association Between DNA and RNA Oxidative Damage and Mortality of Patients with Traumatic Brain Injury

被引：13

作者：

Lorente, Leonardo ^{[1
]}

Martin, Maria M. ^{[2
]}

Gonzalez-Rivero, Agustin F. ^{[3
]}

Perez-Cejas, Antonia ^{[3
]}

Abreu-Gonzalez, Pedro ^{[4
]}

Ramos, Luis ^{[5
]}

Argueso, Monica ^{[6
]}

Caceres, Juan J. ^{[7
]}

Sole-Violan, Jordi ^{[8
]}

Alvarez-Castillo, Andrea ^{[1
]}

Jimenez, Alejandro ^{[9
]}

Garcia-Marin, Victor ^{[10
]}

机构：

[1] Hosp Univ Canarias, Intens Care Unit, Ofra S-N, San Cristobal la Laguna 38320, Santa Cruz De T, Spain

[2] Hosp Univ Nuestra Senora Candelaria, Intens Care Unit, Crta Rosario S-N, Santa Cruz De Tenerife 38010, Spain

[3] Hosp Univ Canarias, Lab Dept, Ofra S-N, San Cristobal la Laguna 38320, Santa Cruz De T, Spain

[4] Univ La Laguna, Fac Med, Dept Physiology, Ofra S-N, San Cristobal la Laguna 38320, Santa Cruz De T, Spain

[5] Hosp Gen La Palma, Intens Care Unit, Buenavista Arriba S-N, Brena Alta 38713, La Palma, Spain

[6] Hosp Clin Univ Valencia, Intens Care Unit, Avda Blasco Ibanez 17-19, Valencia 46004, Spain

[7] Hosp Insular, Intens Care Unit, Plaza Dr Pasteur S-N, Las Palmas Gran Canaria 35016, Spain

[8] Hosp Univ Dr Negrin, Intens Care Unit, Barranco Ballena S-N, Las Palmas Gran Canaria 35010, Spain

[9] Hosp Univ Canarias, Res Unit, Ofra S-N, San Cristobal la Laguna 38320, Santa Cruz De T, Spain

[10] Hosp Univ Canarias, Dept Neurosurg, Ofra S-N, San Cristobal la Laguna 38320, Santa Cruz De T, Spain

来源：

NEUROCRITICAL CARE | 2020年 / 32卷 / 03期

基金：

英国科研创新办公室;

关键词：

DNA and RNA oxidative damage; Traumatic brain injury; Mortality; Outcome; 8-HYDROXY-2-DEOXYGUANOSINE LEVELS; STRESS; CLASSIFICATION; DISEASE; METAANALYSIS; SEVERITY; ACID; COMA;

D O I：

10.1007/s12028-019-00800-w

中图分类号：

R4 [临床医学];

学科分类号：

1002 ; 100602 ;

摘要：

Background The 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. Methods We 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. Results We 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). Conclusions To 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.

引用

页码：790 / 795

页数：6

共 35 条

[1] Excessive Reactive Oxygen Species and Exotic DNA Lesions as an Exploitable Liability [J].