Cerebrospinal fluid superoxide dismutase and serum malondialdehyde levels in patients with aneurysmal subarachnoid hemorrhage: preliminary results

Kaynar, Mehmet Yaşar; Tanrıverdi, Taner; Kemerdere, Rahşan; Atukeren, Pınar; Gümüştaş, Koray

doi:10.1179/016164105x17288

Cited by 36 publications

(25 citation statements)

References 37 publications

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“…Oxidative stress has been proven to play a crucial role in the pathophysiological process after SAH. 1,10,14 It has been demonstrated that excessive reactive oxygen species and reactive nitrogen species including hydroxyl radical, superoxide anion, H 2 O 2 , nitric oxide, and peroxynitrite are generated early after SAH, and consume enzymatic and nonenzymatic antioxidant defense systems. 1,20 Moreover, these free radicals will lead to neuronal damage by promoting lipid peroxidation, protein breakdown, and DNA damage, and this in turn leads to cellular apoptosis, endothelial injury, and BBB permeability.…”

Section: Discussionmentioning

confidence: 99%

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Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Zhang

Zhou

et al. 2014

JNS

102

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Object Aneurysmal subarachnoid hemorrhage (SAH) causes devastating rates of mortality and morbidity. Accumulating studies indicate that early brain injury (EBI) greatly contributes to poor outcomes after SAH and that oxidative stress plays an important role in the development of EBI following SAH. Astaxanthin (ATX), one of the most common carotenoids, has a powerful antioxidative property. However, the potential role of ATX in protecting against EBI after SAH remains obscure. The goal of this study was to assess whether ATX can attenuate SAH-induced brain edema, blood-brain barrier permeability, neural cell death, and neurological deficits, and to elucidate whether the mechanisms of ATX against EBI are related to its powerful antioxidant property. Methods Two experimental SAH models were established, including a prechiasmatic cistern SAH model in rats and a one-hemorrhage SAH model in rabbits. Both intracerebroventricular injection and oral administration of ATX were evaluated in this experiment. Posttreatment assessments included neurological scores, body weight loss, brain edema, Evans blue extravasation, Western blot analysis, histopathological study, and biochemical estimation. Results It was observed that an ATX intracerebroventricular injection 30 minutes post-SAH could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological dysfunction) after SAH in rats. Meanwhile, delayed treatment with ATX 3 hours post-SAH by oral administration was also neuroprotective in both rats and rabbits. In addition, the authors found that ATX treatment could prevent oxidative damage and upregulate the endogenous antioxidant levels in the rat cerebral cortex following SAH. Conclusions These results suggest that ATX administration could alleviate EBI after SAH, potentially through its powerful antioxidant property. The authors conclude that ATX might be a promising therapeutic agent for EBI following SAH.

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Section: Discussionmentioning

confidence: 99%

“…1,10,14 Given that there is substantial evidence for significant levels of oxidative stress following SAH and for the beneficial effects of antioxidant therapy in experimental SAH and clinical trials, the use of free-radical scavengers is a reasonable approach in the treatment of SAH.…”

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confidence: 99%

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Zhang

Zhou

et al. 2014

JNS

102

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“…Several studies have suggested that dietary antioxidants may play a protective role against the development of subarachnoid hemorrhage (SAH) (Marzatico et al, 1998;Leppala et al, 1999Leppala et al, , 2000Hirvonen et al, 2000;Kaynar et al, 2005;Okamoto, 2006;Okamoto and Horisawa, 2006). In general, various dietary antioxidants may be interactive or synergistic rather than isolated.…”

Section: Introductionmentioning

confidence: 99%

Dietary antioxidant intake and risk of an aneurysmal rupture subarachnoid hemorrhage in Japan

Okamoto

Horisawa

2007

Eur J Clin Nutr

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The purpose of this study was to investigate the relationship between dietary antioxidant intake and the risk of subarachnoid hemorrhage (SAH) in a case-control study. An antioxidant intake score was calculated for individual values for each food group (soy products, green yellow-vegetables, fruits, boiled rice and tea) collected by a self-administered food frequency questionnaire. Incident SAH cases (n ¼ 201) were identified and individually matched for age (72 years) and gender to community (n ¼ 201) controls from April 1992 to March 1997. The antioxidant intake score was inversely associated with the risk of SAH, even after adjusting for confounding factors (lowest vs highest score adjusted odds ratio, 0.54; 95% confidence interval, 0.30-0.99). These findings suggest that the development of SAH may be reduced by the frequent intake of various antioxidants in the diet. Prospective studies are needed to confirm the relationship of dietary antioxidants to SAH risk in Japanese men and women.

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“…1 Before moving into clinical trials, however, we need to address the possible brain oxidative stress related to HBO because extensive oxidative stress has been reported in SAH animal models, 2 in SAH patients, 3 and application of HBO may potentiate an existing oxidative stress after SAH. Three groups of contradicting reports of HBO in oxidative stress have been published; they state that HBO at pressures higher than 4 atmospheres absolutes (Ͼ4 ATA) increases oxidative stress, 4 but at a lower atmosphere (Յ3 ATA) does not enhance oxidative stress.…”

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confidence: 99%

Hyperbaric Oxygen Suppresses NADPH Oxidase in a Rat Subarachnoid Hemorrhage Model

Ostrowski

Tang

Zhang

2006

Stroke

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Background and Purpose-One of the major contributors to brain injury after subarachnoid hemorrhage (SAH) is oxidative stress, and 1 of the major enzymatic sources of superoxide anion production in the brain is NADPH oxidase. Therefore, we studied whether hyperbaric oxygen (HBO) suppresses neuronal NADPH oxidase in a rat model of SAH. Methods-Eighty-three Sprague-Dawley male rats were assigned to sham, SAH, and SAH treated with HBO groups. SAH was induced by endovascular perforation. HBO (2.8 atmospheres absolutes for 2 hours) was started at 1 hour after perforation. Rats were euthanized at 6 or 24 hours, and brains were collected for histology, biochemistry, and molecular biology studies including NADPH oxidase activity, gp91 phox mRNA expression, and lipid peroxidation assays. Mortality and neurological scores were evaluated. Results-We observed an increased neuronal immunoreactivity of gp91 phox at 24 hours after SAH. The upregulation of gp91 phox mRNA was associated with increased oxidative stress. HBO decreased NADPH oxidase expression, activity, and the level of oxidative stress at 24 hours after SAH. HBO reduced neuronal injury and improved functional performance throughout the observation period. Conclusion-HBO suppresses NADPH oxidase and oxidative stress in cerebral tissues at 24 hours after SAH. (Stroke.2006;37:1314-1318.)

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Cerebrospinal fluid superoxide dismutase and serum malondialdehyde levels in patients with aneurysmal subarachnoid hemorrhage: preliminary results

Abstract: These preliminary results suggest that the levels of antioxidants are decreased after the onset of SAH in the early period, possibly because of increased oxidative stress. Reactive oxygen-mediated oxidative damage may play an important role in inflammation after SAH.

Cited by 36 publications

References 37 publications

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Amelioration of oxidative stress and protection against early brain injury by astaxanthin after experimental subarachnoid hemorrhage

Dietary antioxidant intake and risk of an aneurysmal rupture subarachnoid hemorrhage in Japan

Hyperbaric Oxygen Suppresses NADPH Oxidase in a Rat Subarachnoid Hemorrhage Model

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