TERRENCE MONKS

Summary

Affiliation: University of Arizona
Country: USA

Publications

  1. ncbi The role of metabolism in 3,4-(+)-methylenedioxyamphetamine and 3,4-(+)-methylenedioxymethamphetamine (ecstasy) toxicity
    Terrence J Monks
    Center for Cellular and Molecular Toxicology, College of Pharmacy, University of Texas at Austin, Austin, TX 78712 1074, USA
    Ther Drug Monit 26:132-6. 2004
  2. ncbi Accumulation of neurotoxic thioether metabolites of 3,4-(+/-)-methylenedioxymethamphetamine in rat brain
    Gladys V Erives
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, 1703 E Mabel Street, Tucson, AZ 85721 0207, USA
    J Pharmacol Exp Ther 324:284-91. 2008
  3. ncbi Thioether metabolites of 3,4-methylenedioxyamphetamine and 3,4-methylenedioxymethamphetamine inhibit human serotonin transporter (hSERT) function and simultaneously stimulate dopamine uptake into hSERT-expressing SK-N-MC cells
    Douglas C Jones
    Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, USA
    J Pharmacol Exp Ther 311:298-306. 2004
  4. ncbi Serotonergic neurotoxic metabolites of ecstasy identified in rat brain
    Douglas C Jones
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, AZ 85721-0207, USA
    J Pharmacol Exp Ther 313:422-31. 2005
  5. ncbi Hepatotoxicity of 3,4-methylenedioxyamphetamine and alpha-methyldopamine in isolated rat hepatocytes: formation of glutathione conjugates
    Márcia Carvalho
    REQUIMTE, Toxicology Department, Faculty of Pharmacy, University of Porto, Rua Anibal Cunha 164, 4050 047 Porto, Portugal
    Arch Toxicol 78:16-24. 2004
  6. ncbi EGFR-independent activation of p38 MAPK and EGFR-dependent activation of ERK1/2 are required for ROS-induced renal cell death
    Jing Dong
    Dept. of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, AZ 85721, USA
    Am J Physiol Renal Physiol 287:F1049-58. 2004
  7. ncbi Introduction
    Terrence J Monks
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, Arizona 85721, USA
    Drug Metab Rev 38:599-600. 2006
  8. ncbi Mitogen-activated protein kinases contribute to reactive oxygen species-induced cell death in renal proximal tubule epithelial cells
    Sampath Ramachandiran
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA
    Chem Res Toxicol 15:1635-42. 2002
  9. ncbi Ros-induced histone modifications and their role in cell survival and cell death
    Terrence J Monks
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, Arizona 85721 0207, USA
    Drug Metab Rev 38:755-67. 2006
  10. ncbi 2,3,5-tris(Glutathion-S-yl)hydroquinone (TGHQ)-mediated apoptosis of human promyelocytic leukemia cells is preceded by mitochondrial cytochrome c release in the absence of a decrease in the mitochondrial membrane potential
    Mi Young Yang
    Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA
    Toxicol Sci 86:92-100. 2005

Research Grants

  1. PATHWAYS TO ROS INDUCED CELL DEATH
    TERRENCE MONKS; Fiscal Year: 2006
  2. Hepatic Metabolism and Susceptibility to Ecstasy Toxicity
    TERRENCE MONKS; Fiscal Year: 2009
  3. BENZENE METABOLITES AND HEMATOTOXICITY
    TERRENCE MONKS; Fiscal Year: 2004
  4. Hepatic Metabolism and Susceptibility to Ecstasy Toxicity
    Terrence J Monks; Fiscal Year: 2010

Collaborators

  • D Li
  • Kulbhushan Tikoo
  • Samy L Habib
  • Serrine S Lau
  • Jing Dong
  • Douglas C Jones
  • Sampath Ramachandiran
  • Hae Seong Yoon
  • Márcia Carvalho
  • Zhe Jia
  • Maria D Person
  • Gladys V Erives
  • Andrew J Slot
  • Mi Young Yang
  • Maria Elena Reveron
  • Hae-Seong Yoon
  • Jeffrey I Everitt
  • Felix Carvalho
  • Maria Lourdes Bastos
  • Fernanda Borges
  • Eduarda Fernandes
  • Nuno Milhazes
  • Susan P C Cole
  • Dana D Wise
  • Roger G Deeley
  • Christine L Duvauchelle
  • Rafael de la Torre
  • Aiko Ikegami
  • Christopher M Olsen
  • Christine Duvauchelle
  • Francisco Amado
  • Fernando Remião
  • Mary Anne S Chacko
  • Jianjm Shen
  • Sean C Hensley
  • James L Stevens
  • Gabrielle Hawksworth
  • Cheryl L Walker
  • Qihong Huang

Detail Information

Publications20

  1. ncbi The role of metabolism in 3,4-(+)-methylenedioxyamphetamine and 3,4-(+)-methylenedioxymethamphetamine (ecstasy) toxicity
    Terrence J Monks
    Center for Cellular and Molecular Toxicology, College of Pharmacy, University of Texas at Austin, Austin, TX 78712 1074, USA
    Ther Drug Monit 26:132-6. 2004
    ..The data are consistent with the view that thioether metabolites of alpha-MeDA and N-methyl-alpha-MeDA contribute to the neurotoxicity of the parent amphetamines...
  2. ncbi Accumulation of neurotoxic thioether metabolites of 3,4-(+/-)-methylenedioxymethamphetamine in rat brain
    Gladys V Erives
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, 1703 E Mabel Street, Tucson, AZ 85721 0207, USA
    J Pharmacol Exp Ther 324:284-91. 2008
    ..The data indicate that neurotoxic metabolites of MDMA may accumulate in brain after multiple dosing...
  3. ncbi Thioether metabolites of 3,4-methylenedioxyamphetamine and 3,4-methylenedioxymethamphetamine inhibit human serotonin transporter (hSERT) function and simultaneously stimulate dopamine uptake into hSERT-expressing SK-N-MC cells
    Douglas C Jones
    Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, USA
    J Pharmacol Exp Ther 311:298-306. 2004
    ....
  4. ncbi Serotonergic neurotoxic metabolites of ecstasy identified in rat brain
    Douglas C Jones
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, AZ 85721-0207, USA
    J Pharmacol Exp Ther 313:422-31. 2005
    ..The mechanisms by which such metabolites access the brain and produce selective serotonergic neurotoxicity remain to be determined...
  5. ncbi Hepatotoxicity of 3,4-methylenedioxyamphetamine and alpha-methyldopamine in isolated rat hepatocytes: formation of glutathione conjugates
    Márcia Carvalho
    REQUIMTE, Toxicology Department, Faculty of Pharmacy, University of Porto, Rua Anibal Cunha 164, 4050 047 Porto, Portugal
    Arch Toxicol 78:16-24. 2004
    ..The results provide evidence that one of the early consequences of MDMA metabolism is a disruption of thiol homeostasis, which may result in loss of protein function and the initiation of a cascade of events leading to cellular damage...
  6. ncbi EGFR-independent activation of p38 MAPK and EGFR-dependent activation of ERK1/2 are required for ROS-induced renal cell death
    Jing Dong
    Dept. of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, AZ 85721, USA
    Am J Physiol Renal Physiol 287:F1049-58. 2004
    ..e., histone H3 and Hsp27 phosphorylation, which have in common the potential ability to remodel chromatin...
  7. ncbi Introduction
    Terrence J Monks
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, Arizona 85721, USA
    Drug Metab Rev 38:599-600. 2006
  8. ncbi Mitogen-activated protein kinases contribute to reactive oxygen species-induced cell death in renal proximal tubule epithelial cells
    Sampath Ramachandiran
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA
    Chem Res Toxicol 15:1635-42. 2002
    ..The data provide evidence that the activation of MAPKs by ROS in renal epithelial cells plays an important role in oncotic cell death, and NF-kB is involved in the cytoprotective effects of PD098059...
  9. ncbi Ros-induced histone modifications and their role in cell survival and cell death
    Terrence J Monks
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, Tucson, Arizona 85721 0207, USA
    Drug Metab Rev 38:755-67. 2006
    ..Attempts to determine the precise site of histone H3 phosphorylation, putative histone H3 kinases, and histone H3 interacting proteins are underway...
  10. ncbi 2,3,5-tris(Glutathion-S-yl)hydroquinone (TGHQ)-mediated apoptosis of human promyelocytic leukemia cells is preceded by mitochondrial cytochrome c release in the absence of a decrease in the mitochondrial membrane potential
    Mi Young Yang
    Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA
    Toxicol Sci 86:92-100. 2005
    ..Taken together, we conclude that TGHQ facilitates ROS production, alters the post-translational modification of Bcl-2 and subcellular localization of Bax, culminating in the release of cytochrome c and caspase activation...
  11. ncbi Age-dependent (+)MDMA-mediated neurotoxicity in mice
    Maria Elena Reveron
    Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, TX 78712, USA
    Neurotoxicology 26:1031-40. 2005
    ....
  12. ncbi Grp78 is essential for 11-deoxy-16,16-dimethyl PGE2-mediated cytoprotection in renal epithelial cells
    Zhe Jia
    Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona Health Sciences Center, 1703, E. Mabel St, Tucson, AZ 85721-0207, USA
    Am J Physiol Renal Physiol 287:F1113-22. 2004
    ..The findings suggest that additional proteins may act in concert with Grp78 during DDM-PGE(2)-mediated cytoprotection against oncotic cell death...
  13. ncbi The metabolism and toxicity of quinones, quinonimines, quinone methides, and quinone-thioethers
    Terrence J Monks
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin, Austin, TX 78712 1074, USA
    Curr Drug Metab 3:425-38. 2002
    ..Specific examples will be discussed to illustrate the diverse manner by which quinones interact with biological systems to initiate and propagate a toxic response...
  14. ncbi Induction of ERK1/2 and histone H3 phosphorylation within the outer stripe of the outer medulla of the Eker rat by 2,3,5-tris-(glutathion-S-yl)hydroquinone
    Jing Dong
    Department of Pharmacology and Toxicology, College of Pharmacy, The University of Arizona Health Sciences Center, Tucson, Arizona 85721, USA
    Toxicol Sci 80:350-7. 2004
    ..These data indicate that activation of the ERK1/2 pathway precedes overt cytotoxicity and that the signaling pathways activated by TGHQ in vivo and in vitro differ...
  15. ncbi Tuberous sclerosis-2 tumor suppressor modulates ERK and B-Raf activity in transformed renal epithelial cells
    Hae Seong Yoon
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Texas 78712, USA
    Am J Physiol Renal Physiol 286:F417-24. 2004
    ..The data indicate that loss of tuberin results in the upregulation of the ERK signaling pathway with subsequent increases in new DNA synthesis, and ultimately, tumor formation...
  16. ncbi An integrated approach to identifying chemically induced posttranslational modifications using comparative MALDI-MS and targeted HPLC-ESI-MS/MS
    Maria D Person
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, 78712, USA
    Chem Res Toxicol 16:598-608. 2003
    ..This unpredicted reaction product is characterized using our unbiased methods for detection and demonstrates the important influence of protein structure on chemical adduction...
  17. ncbi Reduced constitutive 8-oxoguanine-DNA glycosylase expression and impaired induction following oxidative DNA damage in the tuberin deficient Eker rat
    Samy L Habib
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX 78712-1074, USA
    Carcinogenesis 24:573-82. 2003
    ..In keeping with this view, acute TGHQ-induced cytotoxicity was greater in Tsc-2(EK/+) rats than in Tsc-2(+/+) rats. The mechanism(s) coupling tuberin expression to the regulation of OGG1 are not known and are under investigation...
  18. ncbi Role of metabolites in MDMA (ecstasy)-induced nephrotoxicity: an in vitro study using rat and human renal proximal tubular cells
    Márcia Carvalho
    CEQUP, Toxicology Department, Faculty of Pharmacy, University of Porto, Rua Anibal Cunha, 164, 4050 047 Porto, Portugal
    Arch Toxicol 76:581-8. 2002
    ..Thus, it appears that toxicity induced by thioether metabolites of ecstasy at the apical membrane of renal proximal tubular cells is the result of extracellular events, presumably redox cycling...
  19. ncbi Cell proliferation is insufficient, but loss of tuberin is necessary, for chemically induced nephrocarcinogenicity
    Hae Seong Yoon
    Center for Molecular and Cellular Toxicology, Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas 78712 1074, USA
    Am J Physiol Renal Physiol 283:F262-70. 2002
    ....
  20. ncbi Modulation of human multidrug resistance protein (MRP) 1 (ABCC1) and MRP2 (ABCC2) transport activities by endogenous and exogenous glutathione-conjugated catechol metabolites
    Andrew J Slot
    Department of Pathology and Molecular Medicine and Division of Cancer Biology and Genetics, Queen s University, Kingston, Ontario, Canada
    Drug Metab Dispos 36:552-60. 2008
    ..In conclusion, we have identified three new classes of MRP1 and MRP2 modulators and demonstrated that one of these, the estrogen conjugates, shows unanticipated differences in their interactions with the two transporters...

Research Grants15

  1. PATHWAYS TO ROS INDUCED CELL DEATH
    TERRENCE MONKS; Fiscal Year: 2006
    ..Basic knowledge of the mechanisms by which ROS induce cell death may yield strategies for clinical interventions in pathologies in which ROS play a prominent role ..
  2. Hepatic Metabolism and Susceptibility to Ecstasy Toxicity
    TERRENCE MONKS; Fiscal Year: 2009
    ....
  3. BENZENE METABOLITES AND HEMATOTOXICITY
    TERRENCE MONKS; Fiscal Year: 2004
    ....
  4. Hepatic Metabolism and Susceptibility to Ecstasy Toxicity
    Terrence J Monks; Fiscal Year: 2010
    ....