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DNA 和 RNA 氧化损伤与创伤性脑损伤患者死亡率的关系。

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

机构信息

Intensive Care Unit, Hospital Universitario de Canarias, Ofra, s/n. La Laguna, 38320, Santa Cruz de Tenerife, Spain.

Intensive Care Unit, Hospital Universitario Nuestra Señora de Candelaria, Crta del Rosario s/n, 38010, Santa Cruz de Tenerife, Spain.

出版信息

Neurocrit Care. 2020 Jun;32(3):790-795. doi: 10.1007/s12028-019-00800-w.

Abstract

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.

摘要

背景

创伤性脑损伤(TBI)中的氧化应激状态可能会对核糖核酸(RNA)和脱氧核糖核酸(DNA)造成氧化损伤。已经研究了 TBI 患者的核酸氧化损伤,并且在 TBI 后死亡的患者的死后大脑样本中发现比因突发性心脏死亡而死亡的患者更高浓度的 8-OHdG。因此,本研究的目的是确定 TBI 患者血清 DNA 和 RNA 氧化损伤与死亡率之间是否存在关联。

方法

我们纳入了严重孤立性 TBI 患者,定义为格拉斯哥昏迷量表(GCS)评分低于 9 分且损伤严重程度评分中非颅方面评分低于 9 分的患者。我们在 TBI 当天测定了三种氧化鸟嘌呤种(OGS)(来自 DNA 的 8-OHdG、来自 RNA 的 8-羟基鸟嘌呤和来自 DNA 或 RNA 的 8-羟基鸟嘌呤)和丙二醛(估计脂质过氧化)的血清浓度。30 天死亡率是终点研究。

结果

我们发现非存活患者(n=34)的血清 OGS(p<0.001)和丙二醛(p<0.001)浓度高于存活患者(n=90),在控制 GCS、年龄和计算机断层扫描发现后,血清 OGS 水平与 30 天死亡率之间存在关联(OR=1.397;95%CI=1.137-1.716;p=0.001),并且血清 OGS 水平与丙二醛之间呈正相关(rho=0.24;p=0.01)。

结论

据我们所知,我们的研究是报告 TBI 患者 DNA 氧化损伤数据的最大系列,并且是首次报告 TBI 患者 DNA 和 RNA 氧化损伤与脂质过氧化和死亡率相关的研究。

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