Arleen Rifkind

Arleen Rifkind received a B.A. degree from Bryn Mawr College and M.D. degree from NYU Medical School. After residency training in internal medicine at Bellevue Hospital in NYC, she spent three years at the NIH as a Clinical Associate (Endocrine Division of the Cancer Institute) where she participated in the discovery that gonadotropins are secreted substantially before puberty. A Research Associateship at Rockefeller University introduced her to her long-term research interests: heme biosynthesis, cytochrome P450, drug metabolism, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD/dioxin) toxicity. She joined Weill/Cornell Medical School where she has been Professor of Pharmacology since 1983. She served on or led several NIH study sections including the Toxicology Study Section and is currently a member of the advisory board of the Wayne State University (Environmental Health Sciences Center). She has been an Associate Editor of Drug Metabolism and Disposition and has served on editorial boards of Biochemical Pharmacology and Toxicology and Applied Pharmacology. Her research and publications have focused on mechanisms of aryl hydrocarbon receptor (AhR) mediated toxicity, roles of cytochrome P4501A induction and mitochondria in TCDD effects, and production of AhR activators by light. She pioneered use of the chick embryo as a model for TCDD toxicity studies. Her group cloned and sequenced the avian CYP1A enzymes, CYPs1A4 and 1A5 and discovered that human CYP1A2 and chick CYP1A5 are highly active arachidonic acid epoxygenases. Her laboratory is currently studying transcriptional and posttranscriptional effects of AhR activation and CYP1A induction leading to dysregulation of signaling pathways governing nutrient and energy metabolism.

Biography Updated on 11 February 2008

Personal Home Page

http://www.med.cornell.edu/research/abrifkind/

Articles in Scholarly Journals [Incomplete List]

  1. Mitochondrial P450-dependent arachidonic acid metabolism by TCDD-induced hepatic CYP1A5; conversion of EETs to DHETs by mitochondrial soluble epoxide hydrolase
    Archives of Biochemistry and Biophysics, vol. 468, no. 1, pp. 70–81, 2007
  2. CYP1A in TCDD Toxicity and in Physiology–with Particular Reference to CYP Dependent Arachidonic Acid Metabolism and other Endogenous Substrates
    Drug Metabolism Reviews, vol. 38, no. 1-2, pp. 291–335, 2006
  3. INDUCTION OF CYP1A AND CYP2-MEDIATED ARACHIDONIC ACID EPOXYGENATION AND SUPPRESSION OF 20-HYDROXYEICOSATETRAENOIC ACID BY IMIDAZOLE DERIVATIVES INCLUDING THE AROMATASE INHIBITOR VOROZOLE
    Drug Metabolism and Disposition, vol. 34, no. 8, pp. 1376–1385, 2006
  4. Sunlight Generates Multiple Tryptophan Photoproducts Eliciting High Efficacy CYP1A Induction in Chick Hepatocytes and In Vivo
    Toxicological Sciences, vol. 90, no. 1, pp. 96–110, 2005
  5. Cell-type specificity of ectonucleotidase expression and upregulation by 2,3,7,8-tetrachlorodibenzo-p-dioxin
    Archives of Biochemistry and Biophysics, vol. 407, no. 1, pp. 49–62, 2002
  6. TCDD Induces CYP1A4 and CYP1A5 in Chick Liver and Kidney and Only CYP1A4, an Enzyme Lacking Arachidonic Acid Epoxygenase Activity, in Myocardium and Vascular Endothelium
    Toxicology and Applied Pharmacology, vol. 164, no. 1, pp. 24–37, 2000
  7. Ventricular Preexcitation Sensitive to Flecainide in Late Stage Chick Embryo ECGs: 2,3,7,8-Tetrachlorodibenzo-p-dioxin Impairs Inotropic but Not Chronotropic or Dromotropic Responses to Isoproterenol and Confers Resistance to Flecainide
    Toxicology and Applied Pharmacology, vol. 166, no. 1, pp. 43–50, 2000
  8. Olfaction and Symptoms in the Multiple Chemical Sensitivities Syndrome, , From the Environmental Health and Safety Council of the American Health Foundation
    Preventive Medicine, vol. 28, no. 5, pp. 467–480, 1999
  9. Transcriptional Activation of AvianCYP1A4andCYP1A5by 2,3,7,8-Tetrachlorodibenzo-p-dioxin: Differences in Gene Expression and Regulation Compared to MammalianCYP1A1andCYP1A2
    Toxicology and Applied Pharmacology, vol. 155, no. 1, pp. 96–106, 1999
  10. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Induces Hepatic Cytochrome P450-Dependent Arachidonic Acid Epoxygenation in Diverse Avian Orders: Regioisomer Selectivity and Immunochemical Comparison of the TCDD-Induced P450s to CYP1A4 and 1A5
    Toxicology and Applied Pharmacology, vol. 150, no. 1, pp. 106–116, 1998
  11. 2,3,7,8-Tetrachlorodibenzo-p-dioxin Induction of Cytochrome P450-Dependent Arachidonic Acid Metabolism in Mouse Liver Microsomes: Evidence for Species-Specific Differences in Responses
    Toxicology and Applied Pharmacology, vol. 153, no. 1, pp. 1–11, 1998
  12. Molecular Cloning and Expression of Two Novel Avian Cytochrome P450 1A Enzymes Induced by 2,3,7,8-Tetrachlorodibenzo-p-dioxin
    Journal of Biological Chemistry, vol. 271, no. 51, pp. 33054–33059, 1996
  13. Arachidonic acid metabolism by human cytochrome P450s 2C8, 2C9, 2E1, and 1A2: Regioselective oxygenation and evidence for a role for CYP2C enzymes in arachidonic acid epoxygenation in human liver microsomes
    Archives of Biochemistry and Biophysics, vol. 320, no. 2, pp. 380–389, 1995
  14. Asbestos in the Air of Public Buildings: A Public Health Risk?
    Preventive Medicine, vol. 23, no. 1, pp. 119–125, 1994
  15. Nitric Oxide is a Mediator of the Decrease in Cytochrome P450-Dependent Metabolism Caused by Immunostimulants
    Proceedings of the National Academy of Sciences, vol. 90, no. 23, pp. 11147–11151, 1993
  16. 2,3,7,8-Tetrachlorodibenzo-p-dioxin increases reliance on fats as a fuel source independently of diet: Evidence that diminished carbohydrate supply contributes to dioxin lethality
    Biochemical and Biophysical Research Communications, vol. 174, no. 3, pp. 1267–1271, 1991
  17. Arachidonic acid metabolism by dioxin-induced cytochrome P-450: A new hypothesis on the role of P-450 in dioxin toxicity
    Biochemical and Biophysical Research Communications, vol. 172, no. 3, pp. 1180–1188, 1990
  18. Nad(P)H:quinone oxidoreductase (DT-diaphorase) in chick embryo liver Comparison to activity in rat and guinea pig liver and differences in co-induction with 7-ethoxyresorufin deethylase by 2,3,7,8-tetrachlorodibenzo-p-dioxin
    Biochemical Pharmacology, vol. 39, no. 2, pp. 327–335, 1990
  19. Heart as a Target Organ in 2,3,7,8-tetrachlorodibenzo-p-dioxin Toxicity: Decreased   -adrenergic Responsiveness and Evidence of Increased Intracellular Calcium
    Proceedings of the National Academy of Sciences, vol. 85, no. 3, pp. 905–909, 1988
  20. Prostaglandin release by the chick embryo heart is increased by 2,3,7,8-tetrachlorodibenzo-p-dioxin and by other cytochrome P-448 inducers
    Biochemical and Biophysical Research Communications, vol. 136, no. 2, pp. 582–589, 1986
  21. Polychlorinated aromatic hydrocarbon lethality, mixed-function oxidase induction, and uroporphyrinogen decarboxylase inhibition in the chick embryo: Dissociation of dose-response relationships*1
    Toxicology and Applied Pharmacology, vol. 78, no. 2, pp. 268–279, 1985
  22. Coordinate induction of cytochrome P-448 mediated mixed function oxidases and histopathologic changes produced acutely in chick embryo liver by polychlorinated biphenyl congeners*1
    Toxicology and Applied Pharmacology, vol. 72, no. 2, pp. 343–354, 1984
  23. Benoxaprofen suppression of polychlorinated biphenyl toxicity without alteration of mixed function oxidase function
    Nature, vol. 303, no. 5917, Article ID 303524a0, 2 pages, 1983
  24. Selective Growth of a Population of Human Basophil Cells in vitro
    Proceedings of the National Academy of Sciences, vol. 78, no. 9, pp. 5793–5796, 1981
  25. Equality of the rates of mixed function oxidation in livers of male and female chick embryos
    Biochemical Pharmacology, vol. 28, no. 10, pp. 1681–1683, 1979
  26. Inhibition of chemical induction of porphyrin synthesis in chick embryo liver cells by partially purified human chorionic gonadotropin
    Biochemical and Biophysical Research Communications, vol. 68, no. 2, pp. 503–510, 1976
  27. Components of the heme biosynthetic pathway and mixed function oxidase activity in human fetal tissues
    Biochemical Pharmacology, vol. 24, no. 8, pp. 839–846, 1975
  28. Teratogenic effects of trimethadione and dimethadione in the chick embryo*1
    Toxicology and Applied Pharmacology, vol. 30, no. 3, pp. 452–457, 1974
  29. PLASMA MEMBRANES OF THE RAT LIVER: Isolation and Enzymatic Characterization of a Fraction Rich in Bile Canaliculi
    The Journal of Cell Biology, vol. 41, no. 1, pp. 124–132, 1969