Tibor Kristian

Summary

Affiliation: University of Maryland
Country: USA

Publications

  1. doi Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection
    Tibor Kristian
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, School of Medicine, University of Maryland Baltimore, Baltimore, Maryland 21201, USA
    J Neurosci Res 89:1946-55. 2011
  2. pmc Hyperoxic reperfusion after global cerebral ischemia promotes inflammation and long-term hippocampal neuronal death
    Julie L Hazelton
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Neurotrauma 27:753-62. 2010
  3. ncbi Methoxychlor inhibits brain mitochondrial respiration and increases hydrogen peroxide production and CREB phosphorylation
    Rosemary A Schuh
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, 21201, USA
    Toxicol Sci 88:495-504. 2005
  4. pmc Visualization and quantification of NAD(H) in brain sections by a novel histo-enzymatic nitrotetrazolium blue staining technique
    Irina S Balan
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, University of Maryland, School of Medicine 685 W Baltimore St, MSTF 5 34, Baltimore, MD 21201, USA
    Brain Res 1316:112-9. 2010
  5. pmc Postischemic oxidative stress promotes mitochondrial metabolic failure in neurons and astrocytes
    Gary Fiskum
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Ann N Y Acad Sci 1147:129-38. 2008
  6. pmc Dietary supplementation with docosahexaenoic acid, but not eicosapentaenoic acid, dramatically alters cardiac mitochondrial phospholipid fatty acid composition and prevents permeability transition
    Ramzi J Khairallah
    Division of Cardiology and Department of Medicine, University of Maryland, 20 Penn Street, HSF2, Room S022, Baltimore, MD 21201, USA
    Biochim Biophys Acta 1797:1555-62. 2010
  7. pmc Cyclophilin D is expressed predominantly in mitochondria of gamma-aminobutyric acidergic interneurons
    Julie L Hazelton
    Department of Anesthesiology Research, School of Medicine, University of Maryland, Baltimore, Maryland 21201, USA
    J Neurosci Res 87:1250-9. 2009
  8. pmc Neuron-specific conditional expression of a mitochondrially targeted fluorescent protein in mice
    Krish Chandrasekaran
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Neurosci 26:13123-7. 2006
  9. pmc Simple model of forebrain ischemia in mouse
    Mitch Onken
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, School of Medicine, University of Maryland Baltimore, 685 West Baltimore Street, MSTF 534, Baltimore, MD 21201, United States
    J Neurosci Methods 204:254-61. 2012
  10. pmc Calcium-induced precipitate formation in brain mitochondria: composition, calcium capacity, and retention
    Tibor Kristian
    Department of Anesthesiology, University of Maryland, School of Medicine, Baltimore, Maryland 21201, USA
    J Neurochem 102:1346-56. 2007

Collaborators

Detail Information

Publications21

  1. doi Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection
    Tibor Kristian
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, School of Medicine, University of Maryland Baltimore, Baltimore, Maryland 21201, USA
    J Neurosci Res 89:1946-55. 2011
    ..These therapeutic approaches are based on utilizing endogenous intermediates of NAD(+) metabolism that feed into the NAD(+) salvage pathway and also inhibit CD38 activity...
  2. pmc Hyperoxic reperfusion after global cerebral ischemia promotes inflammation and long-term hippocampal neuronal death
    Julie L Hazelton
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Neurotrauma 27:753-62. 2010
    ....
  3. ncbi Methoxychlor inhibits brain mitochondrial respiration and increases hydrogen peroxide production and CREB phosphorylation
    Rosemary A Schuh
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, 21201, USA
    Toxicol Sci 88:495-504. 2005
    ..These multiple effects of mxc on mitochondria may play an important role in its toxicity, particularly in the CNS...
  4. pmc Visualization and quantification of NAD(H) in brain sections by a novel histo-enzymatic nitrotetrazolium blue staining technique
    Irina S Balan
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, University of Maryland, School of Medicine 685 W Baltimore St, MSTF 5 34, Baltimore, MD 21201, USA
    Brain Res 1316:112-9. 2010
    ..This new histo-enzymatic technique is suitable for visualizing and quantifying relative NAD(H) levels in the brain. This assay could prove useful in identifying region-selective NAD(H) catabolism that may contribute to neurodegeneration...
  5. pmc Postischemic oxidative stress promotes mitochondrial metabolic failure in neurons and astrocytes
    Gary Fiskum
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Ann N Y Acad Sci 1147:129-38. 2008
    ..These results support the hypothesis that release and or consumption of mitochondrial NAD(H) is at least partially responsible for respiratory inhibition, particularly in neurons...
  6. pmc Dietary supplementation with docosahexaenoic acid, but not eicosapentaenoic acid, dramatically alters cardiac mitochondrial phospholipid fatty acid composition and prevents permeability transition
    Ramzi J Khairallah
    Division of Cardiology and Department of Medicine, University of Maryland, 20 Penn Street, HSF2, Room S022, Baltimore, MD 21201, USA
    Biochim Biophys Acta 1797:1555-62. 2010
    ..In summary, dietary supplementation with DHA but not EPA, profoundly altered mitochondrial phospholipid fatty acid composition and delayed Ca2+-induced MPTP opening...
  7. pmc Cyclophilin D is expressed predominantly in mitochondria of gamma-aminobutyric acidergic interneurons
    Julie L Hazelton
    Department of Anesthesiology Research, School of Medicine, University of Maryland, Baltimore, Maryland 21201, USA
    J Neurosci Res 87:1250-9. 2009
    ....
  8. pmc Neuron-specific conditional expression of a mitochondrially targeted fluorescent protein in mice
    Krish Chandrasekaran
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Neurosci 26:13123-7. 2006
    ..More importantly, the development of Dox-inducible, neuron targeted mito/eYFP transgenic mice offer a unique in vivo model for delineating the participation of neuronal mitochondria in neuronal survival and death...
  9. pmc Simple model of forebrain ischemia in mouse
    Mitch Onken
    Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research, School of Medicine, University of Maryland Baltimore, 685 West Baltimore Street, MSTF 534, Baltimore, MD 21201, United States
    J Neurosci Methods 204:254-61. 2012
    ..This study demonstrates the feasibility of using the described model in mice that can be utilized to examine the effect of new neuroprotective compounds or use transgenic animals to test new hypothesis...
  10. pmc Calcium-induced precipitate formation in brain mitochondria: composition, calcium capacity, and retention
    Tibor Kristian
    Department of Anesthesiology, University of Maryland, School of Medicine, Baltimore, Maryland 21201, USA
    J Neurochem 102:1346-56. 2007
    ..Following MPT and/or depolarization, the release of accumulated Ca(2+) is rapid but incomplete; significant residual calcium in the form of precipitates is retained in damaged mitochondria for prolonged periods...
  11. pmc Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders
    Lucian Soane
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neurosci Res 85:3407-15. 2007
    ..In addition, the relationship between apoptotic signaling cascades and disruption of mitochondrial energy metabolism is considered in light of the fine balance between apoptotic and necrotic neural cell death...
  12. ncbi Heterogeneity of the calcium-induced permeability transition in isolated non-synaptic brain mitochondria
    Tibor Kristian
    Department of Anesthesiology, School of Medicine, University of Maryland, Baltimore, Maryland 21201, USA
    J Neurochem 83:1297-308. 2002
    ....
  13. ncbi Metabolic stages, mitochondria and calcium in hypoxic/ischemic brain damage
    Tibor Kristian
    Anesthesiology Research Laboratories, Department of Anesthesiology, School of Medicine, University of Maryland, 685 W Baltimore Street, MSTF 5 34, Baltimore, MD 21201, USA
    Cell Calcium 36:221-33. 2004
    ..However, it is still not clear which are the key mechanisms that cause mitochondrial dysfunction and lead ultimately to cell death, and which have more secondary nature to brain damage acting as aggravating factors...
  14. pmc The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia
    Zara Mehrabian
    Department of Anesthesiology, University of Maryland School of Medicine, 685 W Baltimore Street, Baltimore, MD 21201, USA
    J Interferon Cytokine Res 27:383-92. 2007
    ..These results suggest that GRIM-19 may play a role in ischemia-induced neuronal cell death...
  15. ncbi A fluorescence-based technique for screening compounds that protect against damage to brain mitochondria
    Tibor Kristian
    Department of Anesthesiology, School of Medicine, University of Maryland, 685 West Baltimore Street, MSTF 5 34, Baltimore, MD 21201, USA
    Brain Res Brain Res Protoc 13:176-82. 2004
    ..These results indicate that the NADH/NAD release assay is a simple, reliable, and sensitive method for detecting mitochondrial damage and for screening of compounds that protect mitochondria from injury...
  16. pmc Calcium-dependent dephosphorylation of brain mitochondrial calcium/cAMP response element binding protein (CREB)
    Rosemary A Schuh
    Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Neurochem 92:388-94. 2005
    ..These results further suggest that mitochondrial CREB is located in the matrix or inner membrane and that a kinase and a calcium-dependent phosphatase regulate its phosphorylation state...
  17. pmc Isolation of mitochondria with high respiratory control from primary cultures of neurons and astrocytes using nitrogen cavitation
    Tibor Kristian
    Department of Anesthesiology, School of Medicine, University of Maryland, 685 West Baltimore Street, MSTF 534, Baltimore, MD 21201, USA
    J Neurosci Methods 152:136-43. 2006
    ..This technique thus will allow examination of mitochondria that are exclusively cell specific in origin...
  18. pmc Postischemic hyperoxia reduces hippocampal pyruvate dehydrogenase activity
    Erica M Richards
    Department of Anesthesiology, University of Maryland, Baltimore, MD 21201, USA
    Free Radic Biol Med 40:1960-70. 2006
    ..These results support the hypothesis that oxidative stress contributes to loss of hippocampal PDHC activity during cerebral ischemia and reperfusion and suggest that PDHC is a target of peroxynitrite...
  19. ncbi Astrocyte mitochondrial mechanisms of ischemic brain injury and neuroprotection
    Linda Bambrick
    Department of Anesthesiology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, Maryland 21201, USA
    Neurochem Res 29:601-8. 2004
    ..The potential for astrocyte mitochondria to serve as targets of neuroprotective interventions is also discussed...
  20. doi Mitochondrial Dysfunction and NAD(+) Metabolism Alterations in the Pathophysiology of Acute Brain Injury
    Katrina Owens
    Veterans Affairs Maryland Health Care System, 10 North Greene Street, Baltimore, MD, 21201, USA
    Transl Stroke Res 4:618-34. 2013
    ..Finally, we discuss the potential effects of downstream products of NAD(+) degradation and associated enzymes as well as the role of NAD(+) resynthesis enzymes as potential therapeutic targets. ..
  21. pmc Isolation of mitochondria from the CNS
    Tibor Kristian
    Department of Anesthesiology, Organized Research Center, School of Medicine, University of Maryland, Baltimore, Maryland, USA
    Curr Protoc Neurosci . 2010
    ..These methods yield mitochondria that exhibit good respiratory coupling and high respiratory rates...