Ketones inhibit mitochondrial production of reactive oxygen species production following glutamate excitotoxicity by increasing NADH oxidation
- 2 March 2007
- journal article
- Published by Elsevier BV in Neuroscience
- Vol. 145 (1), 256-264
- https://doi.org/10.1016/j.neuroscience.2006.11.065
Abstract
No abstract availableKeywords
This publication has 54 references indexed in Scilit:
- Acetoacetate protects neuronal cells from oxidative glutamate toxicityJournal of Neuroscience Research, 2006
- Calorie Restriction Promotes Mitochondrial Biogenesis by Inducing the Expression of eNOSScience, 2005
- Calorie restriction, SIRT1 and metabolism: understanding longevityNature Reviews Molecular Cell Biology, 2005
- Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death?Journal of Neuroscience Research, 2004
- Diazoxide preconditioning protects against neuronal cell death by attenuation of oxidative stress upon glutamate stimulationJournal of Neuroscience Research, 2004
- Glutathione depletion enforces the mitochondrial permeability transition and causes cell death in HL60 cells that overexpress Bcl‐2The FASEB Journal, 2002
- β-Hydroxybutyrate, a Cerebral Function Improving Agent, Protects Rat Brain Against Ischemic Damage Caused by Permanent and Transient Focal Cerebral IschemiaThe Japanese Journal of Pharmacology, 2002
- Glutamate Injury–Induced Epileptogenesis in Hippocampal NeuronsStroke, 2001
- Ketone Bodies, Potential Therapeutic UsesIUBMB Life, 2001
- Effect of β-Hydroxybutyrate, a Cerebral Function Improving Agent, on Cerebral Hypoxia, Anoxia and Ischemia in Mice and RatsThe Japanese Journal of Pharmacology, 2001