Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans

Anders Jorgensen; Jonatan M. Staalsoe; Anja H. Simonsen; Steen G. Hasselbalch; Peter Høgh; Allan Weimann; Henrik E. Poulsen; Neils V. Olsen

doi:10.1080/10715762.2017.1407413

Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans

Anders Jorgensen^*
, Jonatan M. Staalsoe
, Anja H. Simonsen
, Steen G. Hasselbalch
, Peter Høgh
, Allan Weimann
, Henrik E. Poulsen
, Neils V. Olsen

^*Corresponding author for this work

Neurology

Research output: Contribution to journal › Article › Research › peer-review

Abstract

Free radical toxicity is considered as a key mechanism in the neuronal damage occurring after aneurysmal subarachnoid haemorrhage (SAH). We measured markers of DNA and RNA damage from oxidation (8-oxodG and 8-oxoGuo, respectively) in cerebrospinal fluid from 45 patients with SAH on day 1–14 after ictus and 45 age-matched healthy control subjects. At baseline, both markers were significantly increased in patients compared to controls (p values <.001), and exhibited a progressive further increase (to >20-fold above control levels) from day 5–14. None of the markers predicted the occurrence of vasospasms or mortality, although there was a trend that the 8-oxoGuo marker was more strongly associated with mortality than the 8-oxodG marker. We conclude that SAH leads to a massive increase in damage to nucleic acids from oxidative stress, which is likely to play a role in neuronal dysfunction and death. As only patients in need of a ventriculostomy catheter were included in the study, the findings cannot necessarily be extrapolated to all patients with SAH.

Original language	English
Pages (from-to)	51-56
Number of pages	6
Journal	Free Radical Research
Volume	52
Issue number	1
DOIs	https://doi.org/10.1080/10715762.2017.1407413
Publication status	Published - 2 Jan 2018

Funding

The work was performed at Departments of Neuroanaesthesia and Neurosurgery, The Neuroscience Centre, University Hospital of Copenhagen (Rigshospitalet), Copenhagen, Denmark & Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark. The study was funded by grants of the University of Copenhagen, the scientific board of the University Hospital of Copenhagen (Rigshospitalet), Absalonfonden, and the Danish psychiatric society research Fund. The study was funded by grants of the University of Copenhagen, the scientific board of the University Hospital of Copenhagen (Rigshospitalet), Absalonfonden, and the Danish Psychiatric Society Research Fund.

Keywords

Aneurysm
nucleic acids
oxidative stress
subarachnoid haemorrhage
vasospasm

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title = "Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans",

abstract = "Free radical toxicity is considered as a key mechanism in the neuronal damage occurring after aneurysmal subarachnoid haemorrhage (SAH). We measured markers of DNA and RNA damage from oxidation (8-oxodG and 8-oxoGuo, respectively) in cerebrospinal fluid from 45 patients with SAH on day 1–14 after ictus and 45 age-matched healthy control subjects. At baseline, both markers were significantly increased in patients compared to controls (p values <.001), and exhibited a progressive further increase (to >20-fold above control levels) from day 5–14. None of the markers predicted the occurrence of vasospasms or mortality, although there was a trend that the 8-oxoGuo marker was more strongly associated with mortality than the 8-oxodG marker. We conclude that SAH leads to a massive increase in damage to nucleic acids from oxidative stress, which is likely to play a role in neuronal dysfunction and death. As only patients in need of a ventriculostomy catheter were included in the study, the findings cannot necessarily be extrapolated to all patients with SAH.",

keywords = "Aneurysm, nucleic acids, oxidative stress, subarachnoid haemorrhage, vasospasm",

author = "Anders Jorgensen and Staalsoe, \{Jonatan M.\} and Simonsen, \{Anja H.\} and Hasselbalch, \{Steen G.\} and Peter H{\o}gh and Allan Weimann and Poulsen, \{Henrik E.\} and Olsen, \{Neils V.\}",

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AU - Staalsoe, Jonatan M.

AU - Simonsen, Anja H.

AU - Hasselbalch, Steen G.

AU - Høgh, Peter

AU - Weimann, Allan

AU - Poulsen, Henrik E.

AU - Olsen, Neils V.

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N2 - Free radical toxicity is considered as a key mechanism in the neuronal damage occurring after aneurysmal subarachnoid haemorrhage (SAH). We measured markers of DNA and RNA damage from oxidation (8-oxodG and 8-oxoGuo, respectively) in cerebrospinal fluid from 45 patients with SAH on day 1–14 after ictus and 45 age-matched healthy control subjects. At baseline, both markers were significantly increased in patients compared to controls (p values <.001), and exhibited a progressive further increase (to >20-fold above control levels) from day 5–14. None of the markers predicted the occurrence of vasospasms or mortality, although there was a trend that the 8-oxoGuo marker was more strongly associated with mortality than the 8-oxodG marker. We conclude that SAH leads to a massive increase in damage to nucleic acids from oxidative stress, which is likely to play a role in neuronal dysfunction and death. As only patients in need of a ventriculostomy catheter were included in the study, the findings cannot necessarily be extrapolated to all patients with SAH.

AB - Free radical toxicity is considered as a key mechanism in the neuronal damage occurring after aneurysmal subarachnoid haemorrhage (SAH). We measured markers of DNA and RNA damage from oxidation (8-oxodG and 8-oxoGuo, respectively) in cerebrospinal fluid from 45 patients with SAH on day 1–14 after ictus and 45 age-matched healthy control subjects. At baseline, both markers were significantly increased in patients compared to controls (p values <.001), and exhibited a progressive further increase (to >20-fold above control levels) from day 5–14. None of the markers predicted the occurrence of vasospasms or mortality, although there was a trend that the 8-oxoGuo marker was more strongly associated with mortality than the 8-oxodG marker. We conclude that SAH leads to a massive increase in damage to nucleic acids from oxidative stress, which is likely to play a role in neuronal dysfunction and death. As only patients in need of a ventriculostomy catheter were included in the study, the findings cannot necessarily be extrapolated to all patients with SAH.

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KW - vasospasm

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Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans

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