ARTHUR GROLLMAN

Summary

Affiliation: Stony Brook University
Country: USA

Publications

  1. doi request reprint Aristolochic acid nephropathy: Harbinger of a global iatrogenic disease
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, New York 11794, USA
    Environ Mol Mutagen 54:1-7. 2013
  2. ncbi request reprint Academic perspectives on dietary supplements use: the need for new guidelines
    Arthur P Grollman
    State University of New York at Stony Brook, Stony Brook, NY, USA
    Thromb Res 117:185-92; discussion 201-7. 2005
  3. ncbi request reprint Role of environmental toxins in endemic (Balkan) nephropathy. October 2006, Zagreb, Croatia
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA
    J Am Soc Nephrol 18:2817-23. 2007
  4. pmc Aristolochic acid and the etiology of endemic (Balkan) nephropathy
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA
    Proc Natl Acad Sci U S A 104:12129-34. 2007
  5. ncbi request reprint Quantitative determination of aristolochic acid-derived DNA adducts in rats using 32P-postlabeling/polyacrylamide gel electrophoresis analysis
    Huan Dong
    Department of Pharmacological Sciences, State University of New York at Stony Brook, NY, USA
    Drug Metab Dispos 34:1122-7. 2006
  6. pmc Cytochrome P450 1A2 detoxicates aristolochic acid in the mouse
    Thomas A Rosenquist
    Department of Pharmacological Sciences, State University of New York, One Nicolls Road, Stony Brook, NY 11794 8651, USA
    Drug Metab Dispos 38:761-8. 2010
  7. doi request reprint Detoxification of aristolochic acid I by O-demethylation: less nephrotoxicity and genotoxicity of aristolochic acid Ia in rodents
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York, Stony Brook, NY, USA
    Int J Cancer 127:1021-7. 2010
  8. ncbi request reprint Selective toxicity of aristolochic acids I and II
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmaceutical Sciences, State University of New York, Stony Brook, NY 11794 8651, USA
    Drug Metab Dispos 35:1217-22. 2007
  9. ncbi request reprint Identification of tamoxifen-DNA adducts in monkeys treated with tamoxifen
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY 11794 8651, USA
    Cancer Res 63:4402-6. 2003
  10. pmc DNA adducts of aristolochic acid II: total synthesis and site-specific mutagenesis studies in mammalian cells
    Sivaprasad Attaluri
    Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794 3400, USA
    Nucleic Acids Res 38:339-52. 2010

Collaborators

Detail Information

Publications31

  1. doi request reprint Aristolochic acid nephropathy: Harbinger of a global iatrogenic disease
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, New York 11794, USA
    Environ Mol Mutagen 54:1-7. 2013
    ....
  2. ncbi request reprint Academic perspectives on dietary supplements use: the need for new guidelines
    Arthur P Grollman
    State University of New York at Stony Brook, Stony Brook, NY, USA
    Thromb Res 117:185-92; discussion 201-7. 2005
  3. ncbi request reprint Role of environmental toxins in endemic (Balkan) nephropathy. October 2006, Zagreb, Croatia
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA
    J Am Soc Nephrol 18:2817-23. 2007
    ..Public health authorities in countries harboring this disease are encouraged to reduce the potential for dietary exposure to Aristolochia clematitis...
  4. pmc Aristolochic acid and the etiology of endemic (Balkan) nephropathy
    Arthur P Grollman
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA
    Proc Natl Acad Sci U S A 104:12129-34. 2007
    ....
  5. ncbi request reprint Quantitative determination of aristolochic acid-derived DNA adducts in rats using 32P-postlabeling/polyacrylamide gel electrophoresis analysis
    Huan Dong
    Department of Pharmacological Sciences, State University of New York at Stony Brook, NY, USA
    Drug Metab Dispos 34:1122-7. 2006
    ..This study establishes the feasibility of using AA-DNA adducts as intermediate biomarkers of exposure in studies of AA nephropathy and its associated urothelial cancer...
  6. pmc Cytochrome P450 1A2 detoxicates aristolochic acid in the mouse
    Thomas A Rosenquist
    Department of Pharmacological Sciences, State University of New York, One Nicolls Road, Stony Brook, NY 11794 8651, USA
    Drug Metab Dispos 38:761-8. 2010
    ..Differences in bioavailability or hepatic metabolism of AAI, expression of CYP1A2, or efficiency of a competing nitroreduction pathway in vivo may explain the apparent differences between human and rodent sensitivity to AAI...
  7. doi request reprint Detoxification of aristolochic acid I by O-demethylation: less nephrotoxicity and genotoxicity of aristolochic acid Ia in rodents
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York, Stony Brook, NY, USA
    Int J Cancer 127:1021-7. 2010
    ..Therefore, the contribution of AA Ia to renal toxicity is minimum. We conclude the metabolic pathway of converting AA I to AA Ia functions as the detoxification of AA I...
  8. ncbi request reprint Selective toxicity of aristolochic acids I and II
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmaceutical Sciences, State University of New York, Stony Brook, NY 11794 8651, USA
    Drug Metab Dispos 35:1217-22. 2007
    ..We conclude that AA-I and AA-II have similar genotoxic and carcinogenic potential, and, although both compounds are cytotoxic, AA-I is solely responsible for the nephrotoxicity associated with AAN...
  9. ncbi request reprint Identification of tamoxifen-DNA adducts in monkeys treated with tamoxifen
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY 11794 8651, USA
    Cancer Res 63:4402-6. 2003
    ..No TAM-DNA adducts were detected in the kidneys or in any tissues obtained from the unexposed monkey. Our results suggest that women receiving TAM may form genotoxic damage in many organs, including the reproductive organs...
  10. pmc DNA adducts of aristolochic acid II: total synthesis and site-specific mutagenesis studies in mammalian cells
    Sivaprasad Attaluri
    Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794 3400, USA
    Nucleic Acids Res 38:339-52. 2010
    ..The dA adduct is significantly more mutagenic than the dG adduct; both adducts give rise, almost exclusively, to misincorporation of dA, which leads to AL-II-dA-->T and AL-II-dG-->T transversions...
  11. ncbi request reprint Mutagenic properties of 3-(deoxyguanosin-N2-yl)-2-acetylaminofluorene, a persistent acetylaminofluorene-derived DNA adduct in mammalian cells
    Manabu Yasui
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 43:15005-13. 2004
    ....
  12. ncbi request reprint Mutagenic specificity of 2-acetylaminonaphthalene-derived DNA adduct in mammalian cells
    Xingzhi Tan
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, NY 11794 8651, USA
    Chem Biol Interact 152:131-8. 2005
    ..0%), were observed. These results demonstrated that dG-N(2)-AAN is a weak mutagenic lesion in mammalian cells. The influence of 5' flanking sequence context was observed on the mutational frequency and specificity of this adduct...
  13. ncbi request reprint Genotoxic mechanism for the major acrolein-derived deoxyguanosine adduct in human cells
    In Young Yang
    Laboratory of Chemical Biology, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Chem Res Toxicol 15:160-4. 2002
    ..5% in XP-A cells. Thus, the authentic major adduct, gamma-OH-PdG, is less blocking to DNA synthesis and less miscoding than the model adduct, PdG...
  14. ncbi request reprint Translesion synthesis by human DNA polymerase kappa on a DNA template containing a single stereoisomer of dG-(+)- or dG-(-)-anti-N(2)-BPDE (7,8-dihydroxy-anti-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene)
    Naomi Suzuki
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 41:6100-6. 2002
    ..Its relatively low contribution to mutagenicity suggests that other newly discovered DNA polymerase(s) may be involved in mutagenic events attributed to dG-N(2)-BPDE adducts in human cells...
  15. ncbi request reprint Mutagenic events in Escherichia coli and mammalian cells generated in response to acetylaminofluorene-derived DNA adducts positioned in the Nar I restriction enzyme site
    Xingzhi Tan
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 41:14255-62. 2002
    ..3-21%, the higher value at G(2). We conclude from this study that the mutation potential of dG-AAF and dG-AF depends on the structure of the adduct, the sequence context of the lesion, and the host cell used for the experiment...
  16. pmc Stereoselective excision of thymine glycol from oxidatively damaged DNA
    Holly Miller
    Laboratory of Chemical Biology, State University of New York, Stony Brook, NY, USA
    Nucleic Acids Res 32:338-45. 2004
    ..When DNA glycosylases occur as complementary pairs, failure of one or both enzymes to excise their cognate Tg stereoisomer from oxidatively damaged DNA could have deleterious consequences for the cell...
  17. ncbi request reprint Substrate discrimination by formamidopyrimidine-DNA glycosylase: a mutational analysis
    Elena I Zaika
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794, USA
    J Biol Chem 279:4849-61. 2004
    ..His-89 and Lys-217 help determine the specificity of Fpg in recognizing the oxidatively damaged base, while Arg-108 provides specificity for bases positioned opposite the lesion...
  18. ncbi request reprint Combining structural and bioinformatics methods for the analysis of functionally important residues in DNA glycosylases
    Dmitry O Zharkov
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, 11794, USA
    Free Radic Biol Med 32:1254-63. 2002
    ..These results serve as a starting point in planning site-directed mutagenesis experiments to elucidate the functional role of similar and dissimilar residues in DNA repair and other proteins...
  19. ncbi request reprint Molecular simulations reveal a common binding mode for glycosylase binding of oxidatively damaged DNA lesions
    Kun Song
    Department of Chemistry, Stony Brook University, Stony Brook, New York 11794 3400, USA
    J Am Chem Soc 129:14536-7. 2007
    ..In simulations with consensus S77, these lesions adopt very similar binding modes...
  20. ncbi request reprint The novel DNA glycosylase, NEIL1, protects mammalian cells from radiation-mediated cell death
    Thomas A Rosenquist
    Department of Pharmacological Sciences, SUNY Stony Brook, Stony Brook, NY 11794, USA
    DNA Repair (Amst) 2:581-91. 2003
    ..The results of these studies suggest that Neil1 is an essential component of base excision repair in mammalian cells; its presence may contribute to the redundant repair capacity observed in Ogg1 -/- and Nth1 -/- mice...
  21. ncbi request reprint Crystallographic characterization of an exocyclic DNA adduct: 3,N4-etheno-2'-deoxycytidine in the dodecamer 5'-CGCGAATTepsilonCGCG-3'
    Eva Freisinger
    Department of Pharmacological Sciences, Center for Structural Biology, State University of New York at Stony Brook, Stony Brook, NY 11794 5115, USA
    J Mol Biol 329:685-97. 2003
    ..Evaluation of the hydration shell of the duplex with bond valence calculations reveals two sodium ions in the crystal...
  22. pmc Catalytic mechanism of Escherichia coli endonuclease VIII: roles of the intercalation loop and the zinc finger
    Konstantin Y Kropachev
    Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 45:12039-49. 2006
    ..We conclude that the opposite-base specificity of Nei is primarily governed by residues in the Q69-Y71 loop and that both this loop and the zinc finger contribute significantly to the substrate specificity of Nei...
  23. ncbi request reprint Proteomic approach to identification of proteins reactive for abasic sites in DNA
    Robert A Rieger
    Department of Pharmacology, Stony Brook University, Stony Brook, NY 11794, USA
    Mol Cell Proteomics 5:858-67. 2006
    ..We report identification of seven proteins from Escherichia coli (AroF, DnaK, MutM, PolA, TnaA, TufA, and UvrA) and two proteins from bakers' yeast (ARC1 and Ygl245wp) reactive for AP sites in this system...
  24. ncbi request reprint Dynamic behavior of DNA base pairs containing 8-oxoguanine
    Xiaolin Cheng
    Department of Chemistry, Stony Brook University, Stony Brook, New York 11794, USA
    J Am Chem Soc 127:13906-18. 2005
    ..These simulations indicate that both the dynamic and equilibrium behavior of the duplex change as a result of oxidation; these differences may provide valuable new insight into the selective action of enzymes on damaged DNA...
  25. pmc Lesion (in)tolerance reveals insights into DNA replication fidelity
    Eva Freisinger
    Department of Pharmacological Sciences, Center for Structural Biology, SUNY at Stony Brook, Stony Brook, NY, USA
    EMBO J 23:1494-505. 2004
    ..In contrast, the structure of the ternary 8-oxodG:dCTP complex is almost identical to the replicating complex containing unmodified DNA, explaining the relative ease and fidelity by which this lesion is bypassed...
  26. ncbi request reprint Mechanism of frameshift (deletion) generated by acetylaminofluorene-derived DNA adducts in vitro
    Shinya Shibutani
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 43:15929-35. 2004
    ..Taken together, these results support the molecular mechanism for frameshift deletion proposed earlier by Shibutani and Grollman in which direct base insertion precedes misalignment [(1993) J. Biol. Chem. 268, 11703]...
  27. ncbi request reprint Mutagenic potential of benzo[a]pyrene-derived DNA adducts positioned in codon 273 of the human P53 gene
    Huan Dong
    Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794 8651, USA
    Biochemistry 43:15922-8. 2004
    ..Thus, the mutational "hot spot" at codon 273 in P53 may reflect either sequence-specific reactivity of BPDE and/or inefficient repair of BPDE-DNA adducts positioned at this site...
  28. ncbi request reprint Ephedra-free is not danger-free
    Donald M Marcus
    Science 301:1669-71; author reply 1669-71. 2003
  29. ncbi request reprint Chromatin structure regulation in transforming growth factor-beta-directed epithelial-mesenchymal transition
    Miroslav Blumenberg
    Department of Dermatology, New York University School of Medicine, New York, NY 10016, USA
    Cells Tissues Organs 185:162-74. 2007
    ..3B. Finally, we discuss the potential significance of this scenario for EMT in the light of recent findings on gene regulation by histone modifications and chromatin structure changes...
  30. ncbi request reprint Science and government. Review for NCCAM is overdue
    Donald M Marcus
    Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA
    Science 313:301-2. 2006
  31. ncbi request reprint Endemic nephropathy: the case for chronic poisoning by aristolochia
    Tjasa Hranjec
    Department of Nephrology and Arterial Hypertension, University Hospital Center Zagreb, Kispaticeva 12, 10000 Zagreb, Croatia
    Croat Med J 46:116-25. 2005
    ....

Research Grants31

  1. MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORS
    ARTHUR GROLLMAN; Fiscal Year: 2006
    ....
  2. Molecular Pharmacology of Oxidative DNA Damage: Structure and Energetics
    ARTHUR GROLLMAN; Fiscal Year: 2007
    ....
  3. Molecular Pharmacology of Oxidative DNA Damage: Structure and Energetics
    ARTHUR GROLLMAN; Fiscal Year: 2009
    ....
  4. MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORS
    ARTHUR GROLLMAN; Fiscal Year: 1993
    ..These phenomena are fundamental to an understanding of the primary events involved in chemical carcinogenesis...
  5. MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORS
    ARTHUR GROLLMAN; Fiscal Year: 1980
    ..Knowledge of the mode of action suggests new uses and may warn against unsuspected toxicities. Information gained from these studies may provide clues that will lead to the development of new chemotherapeutic agents...
  6. Molecular Pharmacology of Oxidative DNA Damage: Structure and Energetics
    Arthur P Grollman; Fiscal Year: 2010
    ....