The Influence of Oxidative Stress on Neurological Outcomes in Spontaneous Intracerebral Hemorrhage.
Julia Masomi-BornwasserElena KurzChristina FrenzJan SchmittDominik M A WespJochem KönigJohannes LotzFlorian RingelThomas KerzHarald KrenzlinNaureen KericPublished in: Biomolecules (2021)
Spontaneous intracerebral hemorrhage (ICH) causes, besides the primary brain injury, a secondary brain injury (SBI), which is induced, amongst other things, by oxidative stress (OS) and inflammation, determining the patient's outcome. This study aims to assess the impact of OS in plasma and cerebrospinal fluid (CSF) on clinical outcomes in patients with ICH. A total of 19 ICH (volume > 30 cc) patients and 29 control patients were included. From day one until seven, blood and CSF samples were obtained, and ICH volume was calculated. OS markers, like malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-sulfhydryl (GSH), and the total antioxidant status (TAS) were measured. Clinical data on treatment and outcome were determined. Patients with mRS ≤ 4 showed significantly elevated SOD and GSH-Px levels in plasma compared to patients with poor CO (p = 0.004; p = 0.002). Initial increased TAS in plasma and increased MDA in CSF were linked to an unfavorable outcome after six months (p = 0.06, r = 0.45; p = 0.05, r = 0.44). A higher ICH volume was associated with a worse outcome at week six (p = 0.04, r = 0.47). OS plays a significant role in SBI. Larger ICHs, elevated MDA in CSF, and TAS in plasma were associated with a detrimental outcome, whereas higher plasma-SOD and -GSH-Px were associated with a favorable outcome.
Keyphrases
- brain injury
- oxidative stress
- subarachnoid hemorrhage
- cerebrospinal fluid
- end stage renal disease
- ejection fraction
- newly diagnosed
- cerebral ischemia
- chronic kidney disease
- prognostic factors
- randomized controlled trial
- dna damage
- fluorescent probe
- hydrogen peroxide
- breast cancer cells
- clinical trial
- metabolic syndrome
- induced apoptosis
- type diabetes
- signaling pathway
- ischemia reperfusion injury
- endothelial cells
- electronic health record
- endoplasmic reticulum stress
- combination therapy
- anti inflammatory
- insulin resistance