Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans
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Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans. / Jorgensen, Anders; Staalsoe, Jonatan M; Simonsen, Anja H; Hasselbalch, Steen G; Høgh, Peter; Weimann, Allan; Poulsen, Henrik E; Olsen, Neils V.
I: Free Radical Research, Bind 52, Nr. 1, 01.2018, s. 51-56.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Progressive DNA and RNA damage from oxidation after aneurysmal subarachnoid haemorrhage in humans
AU - Jorgensen, Anders
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
PY - 2018/1
Y1 - 2018/1
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.
KW - Journal Article
U2 - 10.1080/10715762.2017.1407413
DO - 10.1080/10715762.2017.1407413
M3 - Journal article
C2 - 29157018
VL - 52
SP - 51
EP - 56
JO - Free Radical Research
JF - Free Radical Research
SN - 1071-5762
IS - 1
ER -
ID: 189623632