Research Topics
| ARTHUR GROLLMANSummaryAffiliation: Stony Brook University Country: USA Publications
Research Grants
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Detail Information
Publications
Aristolochic acid nephropathy: Harbinger of a global iatrogenic diseaseArthur 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....
Academic perspectives on dietary supplements use: the need for new guidelinesArthur P Grollman
State University of New York at Stony Brook, Stony Brook, NY, USA
Thromb Res 117:185-92; discussion 201-7. 2005- Role of environmental toxins in endemic (Balkan) nephropathy. October 2006, Zagreb, CroatiaArthur 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... 
Aristolochic acid and the etiology of endemic (Balkan) nephropathyArthur 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....- Quantitative determination of aristolochic acid-derived DNA adducts in rats using 32P-postlabeling/polyacrylamide gel electrophoresis analysisHuan 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... - Cytochrome P450 1A2 detoxicates aristolochic acid in the mouseThomas 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... - Detoxification of aristolochic acid I by O-demethylation: less nephrotoxicity and genotoxicity of aristolochic acid Ia in rodentsShinya 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... - Selective toxicity of aristolochic acids I and IIShinya 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... - Identification of tamoxifen-DNA adducts in monkeys treated with tamoxifenShinya 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... - DNA adducts of aristolochic acid II: total synthesis and site-specific mutagenesis studies in mammalian cellsSivaprasad 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... - Mutagenic properties of 3-(deoxyguanosin-N2-yl)-2-acetylaminofluorene, a persistent acetylaminofluorene-derived DNA adduct in mammalian cellsManabu 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.... - Mutagenic specificity of 2-acetylaminonaphthalene-derived DNA adduct in mammalian cellsXingzhi 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... - Genotoxic mechanism for the major acrolein-derived deoxyguanosine adduct in human cellsIn-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... - 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... - Mutagenic events in Escherichia coli and mammalian cells generated in response to acetylaminofluorene-derived DNA adducts positioned in the Nar I restriction enzyme siteXingzhi 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... - Stereoselective excision of thymine glycol from oxidatively damaged DNAHolly 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... - Substrate discrimination by formamidopyrimidine-DNA glycosylase: a mutational analysisElena 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... - Combining structural and bioinformatics methods for the analysis of functionally important residues in DNA glycosylasesDmitry 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... - Molecular simulations reveal a common binding mode for glycosylase binding of oxidatively damaged DNA lesionsKun 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... - The novel DNA glycosylase, NEIL1, protects mammalian cells from radiation-mediated cell deathThomas 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... - 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... - Catalytic mechanism of Escherichia coli endonuclease VIII: roles of the intercalation loop and the zinc fingerKonstantin 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... - Proteomic approach to identification of proteins reactive for abasic sites in DNARobert 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... - Dynamic behavior of DNA base pairs containing 8-oxoguanineXiaolin 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... - Lesion (in)tolerance reveals insights into DNA replication fidelityEva 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... - Mechanism of frameshift (deletion) generated by acetylaminofluorene-derived DNA adducts in vitroShinya 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]... - Mutagenic potential of benzo[a]pyrene-derived DNA adducts positioned in codon 273 of the human P53 geneHuan 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... - Ephedra-free is not danger-freeDonald M Marcus
Science 301:1669-71; author reply 1669-71. 2003 - Chromatin structure regulation in transforming growth factor-beta-directed epithelial-mesenchymal transitionMiroslav 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... - Science and government. Review for NCCAM is overdueDonald M Marcus
Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA
Science 313:301-2. 2006 - Endemic nephropathy: the case for chronic poisoning by aristolochiaTjasa Hranjec
Department of Nephrology and Arterial Hypertension, University Hospital Center Zagreb, Kispaticeva 12, 10000 Zagreb, Croatia
Croat Med J 46:116-25. 2005..clematitis during harvesting. This observation supports the hypothesis that aristolochic acid, a major constituent of the seeds, plays a central role in the development of endemic nephropathy...
Research Grants
- MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORSARTHUR GROLLMAN; Fiscal Year: 2006....
- Molecular Pharmacology of Oxidative DNA Damage: Structure and EnergeticsARTHUR GROLLMAN; Fiscal Year: 2007....
- Molecular Pharmacology of Oxidative DNA Damage: Structure and EnergeticsARTHUR GROLLMAN; Fiscal Year: 2009....
- MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORSARTHUR GROLLMAN; Fiscal Year: 1993..These phenomena are fundamental to an understanding of the primary events involved in chemical carcinogenesis...
- MOLECULAR PHARMACOLOGY OF TUMOR AND VIRUS INHIBITORSARTHUR 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...
- Molecular Pharmacology of Oxidative DNA Damage: Structure and EnergeticsArthur P Grollman; Fiscal Year: 2010....