Preconditioning-induced protection against cyanide-induced neurotoxicity is mediated by preserving mitochondrial function

Neurochemistry International

Volumn 40, Issue 4, 2002, Pages 285-293

  Jensen, Mads Skak ^a,b   Ahlemeyer, Barbara ^a   Ravati, Alexander ^a   Thakur, Pratima ^a   Mennel, Hans Dieter ^a   Krieglstein, Josef ^a  

^a PHILIPPS UNIVERSITY MARBURG   (Germany)

^b UNIVERSITY OF COPENHAGEN   (Denmark)

Author keywords

Bcl 2; Bcl xL; Chick neurons; Membrane damage; Mitochondrial membrane potential; Nuclear fragmentation; Protein synthesis; Sodium cyanide

Indexed keywords

4 [5 (4 METHYL 1 PIPERAZINYL)[2,5' BI 1H BENZIMIDAZOL] 2' YL]PHENOL; CYCLOHEXIMIDE; PROTEIN BCL 2; PROTEIN BCL XL; SODIUM CYANIDE;

ANIMAL CELL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CELL DEATH; CHROMATIN CONDENSATION; CONTROLLED STUDY; ELECTRON MICROSCOPY; EMBRYO; EMBRYO CELL; EXPOSURE; INCUBATION TIME; MEMBRANE DAMAGE; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRION; NERVE CELL CULTURE; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; PROTEIN SYNTHESIS; STAINING;

ANIMALS; APOPTOSIS; BCL-X PROTEIN; CELL HYPOXIA; CHICK EMBRYO; CYCLOHEXIMIDE; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG TOLERANCE; ELECTRON TRANSPORT COMPLEX IV; GENE EXPRESSION REGULATION; GENES, BCL-2; MEMBRANE POTENTIALS; MITOCHONDRIA; NEURONS; OXIDATIVE PHOSPHORYLATION; PROTEIN SYNTHESIS INHIBITORS; PROTO-ONCOGENE PROTEINS C-BCL-2; SODIUM CYANIDE; TELENCEPHALON;

EID: 0036162973     PISSN: 01970186     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0197-0186(01)00096-1     Document Type: Article

References (51)

1. Testing drug effects against hypoxic damage of cultured neurons during long-term recovery
2. Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function
3. Subunit-specific interactions of cyanide with the N-methyl-D-aspartate receptor
4. Cyanide induces DNA fragmentation in mammalian cell cultures
5. Pharmacological intervention of cyanide-induced cytotoxicity and DNA damage in isolated rat thymocytes and their protective efficacy in vivo
6. Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator
7. Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization
8. Ischemic tolerance in the brain
9. Caspase inhibition extends the commitment to neuronal death beyond cytochrome c release to the point of mitochondrial depolarization
10. Fluorescent dyes for cell viability: An application on prefixed conditions
11. Alteration of cytosolic calcium levels in PC12 cells by potassium cyanide
12. Reactive oxygen species generated by cyanide-mediated toxicity in rat pheochromocytoma cells
13. Chromatin condensation during apoptosis requires ATP
14. Cyanide metabolism in motor neuron disease
15. L as an inhibitor of cytosolic cytochrome c accumulation in DNA damage-induced apoptosis
16. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
17. Mitochondrial control of cell death
18. Mitochondrial depolarization is not required for neuronal apoptosis
19. Inhibition of mitochondrial ATP generation by nitric oxide switches apoptosis to necrosis
20. The permeability transition pore complex: A target for apoptosis regulation by caspases and Bcl-2-related proteins
21. Activation of NF-κB protects hippocampal neurons against oxidative stress-induced apoptosis: Evidence for induction of manganese superoxide dismutase and suppression of peroxynitrite production and protein tyrosine nitration
22. Cyanide-induced apoptosis and oxidative stress in differentiated PC12 cells
23. Differential susceptibility of brain areas to cyanide involves different modes of cell death
24. Bcl-2 protects neural cells from cyanide/aglycemia-induced lipid oxidation, mitochondrial injury, and loss of viability
25. Intracellular ATP: A switch in the decision between apoptosis and necrosis
26. 2+-dependent and independent release of glutamate from mouse brain slices
27. N-methyl-D-aspartate receptors mediate cyanide-induced cytotoxicity in hippocampal cultures
28. Enhancement of NMDA-mediated responses by cyanide
29. Morphological and biochemical maturation of neurones cultured in the absence of glial cells
30. Changes of the trans-activating potential of AP-l transcription factor during cyclosporin A-induced apoptosis of glioma cells are mediated by phosphorylation and alterations of AP-1 composition
31. Glutamate-induced intracellular calcium changes and neurotoxicity in cortical neurons in vitro: Effect of chemical ischemia
32. Preconditioning-induced neuroprotection is mediated by reactive oxygen species
33. Preconditioning-induced neuroprotection is mediated by reactive oxygen species and activation of the transcription factor NF-κB
34. Bcl-2 family proteins and mitochondria
35. Chemical preconditioning: A cytoprotective strategy
36. Increased hypoxic tolerance by chemical inhibition of oxidative phosphorylation: Chemical preconditioning
37. Cyanide-induced Parkinsonism, clinical, MRI, and 6-fluorodopa PET studies
38. Release of apoptogenic proteins from the mitochondrial intermembrane space during the mitochondrial permeability transition
39. NMDA-induced superoxide production and neurotoxicity in cultured rat hippocampal neurons: Role of mitochondria
40. Increase in Bcl-2 oncoprotein and the tolerance to ischemia-induced neuronal death in the gerbil hippocampus
41. Bcl-2 blocks loss of mitochondrial membrane potential while ICE inhibitors act at a different step during inhibition of death induced by respiratory chain inhibitors
42. Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
43. Cyanide-induced apoptosis involves oxidative-stress-activated NF-κB in cortical neurons
44. Cyanide interaction with redox modulatory sites enhances NMDA receptor responses
45. Apoptosis in neurodegenerative diseases: The role of mitochondria
46. Delayed cyanide-induced dystonia
47. Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process
48. Cyanide in human diseases
49. Cyanide-stimulated inositol 1,4,5-trisphosphate formation: An intracellular neurotoxic signaling cascade
50. Prevention of apoptosis by Bcl-2: Release of cytochrome c from mitochondria blocked
51. 2+ block at the N-methyl-D-aspartate receptor underlies receptor activation during inhibition of neuronal metabolism