Arthur I Cederbaum, PhD
- PROFESSOR | Pharmacological Sciences
Research Topics:
Apoptosis/Cell Death, Cytokines, Enzymology, Glutathione, Heme Proteins, Liver, Macrophage, Mitochondria, Oxidative Stress, Protein DegradationDr. Cederbaum is a Professor in the Department of Pharmacology and Systems Therapeutics and Co-Director of the Mount Sinai Liver Disease Research Center.
Multi-Disciplinary Training Area
Pharmacology and Therapeutics Discovery [PTD]Education
Fellowship, Princeton University
PhD, Rutgers University
Fellowship, Mount Sinai School of Medicine
-
2016
Lifetime Achievement Award -
2016
Hiromasa Ishii Memorial Award -
2015
Dr. Arthur Aufses, Jr. Career Achievement Award in Education -
2011
Lifetime Achievement Award -
2009
Mount Sinai Alumni Award for Achievement in Medical Education -
2009
Dean’s Award for Excellence in Basic Science Research -
2008
Mount Sinai Faculty Council Award for Academic Excellence -
2005
Long Island University Brooklyn College of Pharmacy-Distinguished Alumni Award -
2003
Ronald G. Thurman Lectureship Award -
1993
Outstanding Faculty Achievement Award Basic Sciences -
1990
Excellence in Teaching Medical School -
1990
MERIT AWARD
Summary of Research Studies:
The main research efforts are to evaluate the production of an increased state of oxidative stress by ethanol, and the role of reactive oxygen species in the hepatotoxicity produced by ethanol. We are focusing on the ability of ethanol to increase the levels of a cytochrome P450 isoform called CYP2E1, which has been shown to be powerful producer of superoxide radical and H2O2. We have developed stable HepG2 cell lines which over-express CYP2E1 and have shown that ethanol produces cytotoxicity in cells expressing CYP2E1, but not cells lacking CYP2E1. The cytotoxicity is apoptotic in nature and can be prevented by a variety of antioxidants, inhibitors of CYP2E1, caspase 3 inhibitors and transfection with a plasmid which expresses bcl-2. Ethanol toxicity is enhanced by administration of polyunsaturated fatty acids or by iron, which promote lipid peroxidation. Impairment of mitochondrial function is an early step in the CYP2E1 plus ethanol toxicity. The role of calcium in! the overall mechanism of toxicity and up-regulation of protective factors such as glutathione and antioxidants is under evaluation. Protection by adenoviral vectors expressing antioxidant enzymes such as catalase has been demonstrated. We are currently co-incubating our CYP2E1 cell lines with stellate or Kupffer cells to evaluate possible activation of collagen or cytokine production. Reactive oxygen species are detected by ESR spectroscopy but new HPLC spin-trapping methods have been developed which are more sensitive and we are characterizing the utility of these new approaches. A major mechanism by which ethanol enhances the level of CYP2E1 is by stabilizing the enzyme against degradation. We are characterizing this degradation process and the role of the proteasome-ubiquitin system, and molecular chaperones.
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Dr. Cederbaum is not currently required to report Industry relationships.
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