ArticleNeurochemical research2005
Changes of endogenous antioxidant enzymes during ischemic tolerance acquisition.
Article in Neurochemical research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 61 citations in OpenAlex.
- Reduced ischemia-reperfusion oxidative stress injury by melatonin and N-acetylcysteine in the male rat brain.IBRO neuroscience reports · 2024Article
- Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion.European journal of histochemistry : EJH · 2019Article
- Regulation of gene expression in ischemic preconditioning in the brain.Conditioning medicine · 2017Article
- Effect of Hyperhomocysteinemia on Redox Balance and Redox Defence Enzymes in Ischemia-Reperfusion Injury and/or After Ischemic Preconditioning in Rats.Cellular and molecular neurobiology · 2017Article
- Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke.Experimental neurology · 2015Review
- Scheme of Ischaemia-triggered Agents during Brain Infarct Evolution in a Rat Model of Permanent Focal Ischaemia.Journal of molecular neuroscience : MN · 2015Article
- Novel Cellular Mechanisms for Neuroprotection in Ischemic Preconditioning: A View from Inside Organelles.Frontiers in neurology · 2015Review
- The Role of NMDA Receptors in the Development of Brain Resistance through Pre- and Postconditioning.Aging and disease · 2014Review
- The effect of regular exercise on antioxidant enzyme activities and lipid peroxidation levels in both hippocampi after occluding one carotid in rat.The journal of physiological sciences : JPS · 2014Article
- Aminoguanidine administration ameliorates hippocampal damage after middle cerebral artery occlusion in rat.Neurochemical research · 2011Article
- Rosuvastatin induces delayed preconditioning against L-glutamate excitotoxicity in cultured cortical neurons.Neurochemistry international · 2010Article
- Effect of noradrenalin and EGb 761 pretreatment on the ischemia-reperfusion injured spinal cord neurons in rabbits.Cellular and molecular neurobiology · 2009Article
- Molecular mechanisms leading to neuroprotection/ischemic tolerance: effect of preconditioning on the stress reaction of endoplasmic reticulum.Cellular and molecular neurobiology · 2009Article
- Transient forebrain ischemia impact on lymphocyte DNA damage, glutamic acid level, and SOD activity in blood.Cellular and molecular neurobiology · 2009Article
- Effect of antioxidant treatment in global ischemia and ischemic postconditioning in the rat hippocampus.Cellular and molecular neurobiology · 2009Article
- Alterations induced by ischemic preconditioning on secretory pathways Ca2+-ATPase (SPCA) gene expression and oxidative damage after global cerebral ischemia/reperfusion in rats.Cellular and molecular neurobiology · 2009Article
- Region-specific sensitivity of the spinal cord to ischemia/reperfusion: the dynamic of changes in catalytic NOS activity.The journal of physiological sciences : JPS · 2009Article
- Ischemic tolerance as an active and intrinsic neuroprotective mechanism.Handbook of clinical neurology · 2009Review
- Effect of bilateral in vivo ischemia/reperfusion on the activities of superoxide dismutase and catalase: response to a standardized grape suspension.Molecular and cellular biochemistry · 2007Article
- Ischemic preconditioning reduces the severity of ischemia-reperfusion injury of peripheral nerve in rats.Journal of brachial plexus and peripheral nerve injury · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to investigate the role of superoxide dismutase (SOD) and catalase (CAT) in brain ischemic tolerance induced by ischemic preconditioning. Forebrain cerebral ischemia was induced in rat by four vessel occlusion. The activities of the antioxidant enzymes CuZn-SOD, Mn-SOD and CAT were measured in the hippocampus, striatum and cortex after 5 min of ischemia used as a preconditioning and subsequent reperfusion, by spectrophotometric methods. In all ischemia-reperfusion groups (5 h, 1 and 2 days of reperfusion), CuZn-SOD activities were found to be increased if compared to the sham operated controls. The increase was significant (P < 0.05) in all reperfusion groups, particularly after 5 h of reperfusion (3 times) in all studied brain regions; the largest increase was detected in the more vulnerable hippocampus and striatum. Very similar changes were found in Mn-SOD activity. The activity of CAT was increased too, but reached the peak of postischemic activity 24 h after ischemia. Our attempt to understand the mechanisms of increased SOD and CAT activities by application of protein synthesis inhibitor cycloheximide showed that this increase was caused by de novo synthesis of enzymes during first hours after ischemia. Our findings indicate that both major endogenous antioxidant enzymes SOD and CAT are synthesized as soon as 5 h after ischemia. In spite of significant upregulation of these enzymes a large number of neurons in selectively vulnerable CA1 region of hippocampus undergoes to neurodegeneration within 7 days after ischemia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.