Kainic acid-induced lipid peroxidation: protection with butylated hydroxytoluene and U78517F in primary cultures of cerebellar granule cells.
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Summary
Data provide further evidence that the generation of free radicals, subsequently leading to membrane disruption, is central to the mechanism of KA-elicited neuronal death in cultures of cerebellar granule cells.
- Type
- article
- Published
- 1993-10-08
- Cited by
- 96
- References
- 20
- OpenAlex
- https://openalex.org/W1979689412
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:20380181
Keywords
Lipid peroxidation, Butylated hydroxytoluene, Biochemistry, Chemistry, Antioxidant
References
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- Hydrogen peroxide production during experimental protein glycation
- Dissociation of nitric oxide generation and kainate-mediated neuronal degeneration in primary cultures of rat cerebellar granule cells.
- Idebenone attenuates neuronal degeneration induced by intrastriatal injection of excitotoxins.
- Superoxide‐dependent production of hydroxyl radical catalyzed by iron—EDTA complex
- Mechanism of Kainate Toxicity to Cerebellar Neurons In Vitro Is Analogous to Reperfusion Tissue Injury
- Susceptibility of glutathione peroxidase to proteolysis after oxidative alteration by peroxides and hydroxyl radicals.
- Free radicals alter ionic calcium levels and membrane phospholipids in cultured rat ventricular myocytes.
- The measurement and mechanism of lipid peroxidation in biological systems.
- Antioxidants protect against glutamate-induced cytotoxicity in a neuronal cell line.
- U-78517F: a potent inhibitor of lipid peroxidation with activity in experimental brain injury and ischemia.
- Lactic Dehydrogenase Activity in Blood.∗
- Free radicals in biology and medicine
Cited by
- Bioenergetic and oxidative stress in neurodegenerative diseases.
- Markers of glutamatergic neurotransmission and oxidative stress associated with tardive dyskinesia.
- Co-Administration of Acetyl-11-Keto-β-Boswellic Acid, a Specific 5-Lipoxygenase Inhibitor, Potentiates the Protective Effect of COX-2 Inhibitors in Kainic Acid-Induced Neurotoxicity in Mice
- New horizons in molecular mechanisms underlying Parkinson's disease and in our understanding of the neuroprotective effects of selegiline.
- NBQX Treatment Improves Mitochondrial Function and Reduces Oxidative Events after Spinal Cord Injury
- Effects of glutathione depletion by 2‐cyclohexen‐1‐one on excitatory amino acids‐induced enhancement of activator protein‐1 DNA binding in murine hippocampus
- Dependence of excitotoxic neurodegeneration on mitochondrial aconitase inactivation
- Over‐expression of antioxidant enzymes protects cultured hippocampal and cortical neurons from necrotic insults
- Propofol post‐conditioning induced long‐term neuroprotection and reduced internalization of AMPAR GluR2 subunit in a rat model of focal cerebral ischemia/reperfusion
- Melatonin reduces kainate‐induced lipid peroxidation in homogenates of different brain regions
- Effects of nimesulide on kainate-induced in vitro oxidative damage in rat brain homogenates
- Enabling dual cellular destinations of polymeric nanoparticles for treatment following partial injury to the central nervous system.
- Melatonin maintains glutathione homeostasis in kainic acid‐exposed rat brain tissues
- Fresh green tea and gallic acid ameliorate oxidative stress in kainic acid-induced status epilepticus.
- In Vitro and In Vivo Protective Effects of Melatonin against Glutamate Oxidative Stress and Neurotoxicity a
- Inhibition of Cell Cycle Pathway by Flavopiridol Promotes Survival of Cerebellar Granule Cells after an Excitotoxic Treatment
- Clusterin gene expression mediates resistance to apoptotic cell death induced by heat shock and oxidative stress.
- Study of nutraceutical, nutricosmetics and cosmeceutical potentials of polyphenolic bark extracts from Canadian forest species
- Glutamate neurotoxicity, oxidative stress and mitochondria
- Effects of kainic acid lesioning on poly(ADP-ribose) polymerase (PARP) activity in the rat striatum in vivo
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