Mohamed B Abou-Donia

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. ncbi request reprint Neurotoxicity resulting from coexposure to pyridostigmine bromide, deet, and permethrin: implications of Gulf War chemical exposures
    M B Abou-Donia
    Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health 48:35-56. 1996
  2. ncbi request reprint Sensorimotor deficits and increased brain nicotinic acetylcholine receptors following exposure to chlorpyrifos and/or nicotine in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 77:452-8. 2003
  3. doi request reprint Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats
    Mohamed B Abou-Donia
    Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27708, USA
    J Toxicol Environ Health A 71:1415-29. 2008
  4. ncbi request reprint Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, P O Box 3813, Durham, NC 27710, USA
    Pharmacol Biochem Behav 77:253-62. 2004
  5. ncbi request reprint Testicular germ-cell apoptosis in stressed rats following combined exposure to pyridostigmine bromide, N,N-diethyl m-toluamide (DEET), and permethrin
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA
    J Toxicol Environ Health A 66:57-73. 2003
  6. ncbi request reprint Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Pharmacol Biochem Behav 72:881-90. 2002
  7. ncbi request reprint Sensorimotor deficit and cholinergic changes following coexposure with pyridostigmine bromide and sarin in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Toxicol Sci 66:148-58. 2002
  8. ncbi request reprint Effects of daily dermal application of DEET and epermethrin, alone and in combination, on sensorimotor performance, blood-brain barrier, and blood-testis barrier in rats
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 62:523-41. 2001
  9. ncbi request reprint Neurotoxicity of ethyl methacrylate in rats
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 59:97-118. 2000
  10. ncbi request reprint Locomotor and sensorimotor performance deficit in rats following exposure to pyridostigmine bromide, DEET, and permethrin, alone and in combination
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, North Carolina, USA
    Toxicol Sci 60:305-14. 2001

Collaborators

Detail Information

Publications35

  1. ncbi request reprint Neurotoxicity resulting from coexposure to pyridostigmine bromide, deet, and permethrin: implications of Gulf War chemical exposures
    M B Abou-Donia
    Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health 48:35-56. 1996
    ..It also suggests that individuals with low plasma esterase activity may be predisposed to neurologic deficits produced by exposure to certain chemical mixtures...
  2. ncbi request reprint Sensorimotor deficits and increased brain nicotinic acetylcholine receptors following exposure to chlorpyrifos and/or nicotine in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 77:452-8. 2003
    ..These data suggest that exposure to either nicotine or chlorpyrifos or a combination of the two may impair neurobehavioral performance and affect the central nervous system cholinergic pathways...
  3. doi request reprint Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats
    Mohamed B Abou-Donia
    Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27708, USA
    J Toxicol Environ Health A 71:1415-29. 2008
    ....
  4. ncbi request reprint Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, P O Box 3813, Durham, NC 27710, USA
    Pharmacol Biochem Behav 77:253-62. 2004
    ..These results suggest that exposure to various doses of PB, alone and in combination with DEET and permethrin, leads to sensorimotor deficits and differential alterations of the cholinergic system in the CNS...
  5. ncbi request reprint Testicular germ-cell apoptosis in stressed rats following combined exposure to pyridostigmine bromide, N,N-diethyl m-toluamide (DEET), and permethrin
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina, USA
    J Toxicol Environ Health A 66:57-73. 2003
    ..In conclusion, combined exposure to real-life doses of test compounds caused germ-cell apoptosis that was significantly enhanced by stress...
  6. ncbi request reprint Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Pharmacol Biochem Behav 72:881-90. 2002
    ..Ligand binding densities for the m2 muscarinic receptor did not show any change. These results show that low-dose, multiple exposure to uranyl acetate caused prolonged neurobehavioral deficits after the initial exposure has ceased...
  7. ncbi request reprint Sensorimotor deficit and cholinergic changes following coexposure with pyridostigmine bromide and sarin in rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Toxicol Sci 66:148-58. 2002
    ..Furthermore, these results show that treatment with either sarin or PB alone resulted in sensorimotor impairments, while coexposure to high doses of sarin with PB caused an exacerbated deficit...
  8. ncbi request reprint Effects of daily dermal application of DEET and epermethrin, alone and in combination, on sensorimotor performance, blood-brain barrier, and blood-testis barrier in rats
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 62:523-41. 2001
    ..These results show that daily dermal exposure to DEET, alone or in combination with permethrin, decreased BBB permeability in certain brain regions, and impaired sensorimotor performance...
  9. ncbi request reprint Neurotoxicity of ethyl methacrylate in rats
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 59:97-118. 2000
    ....
  10. ncbi request reprint Locomotor and sensorimotor performance deficit in rats following exposure to pyridostigmine bromide, DEET, and permethrin, alone and in combination
    M B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, North Carolina, USA
    Toxicol Sci 60:305-14. 2001
    ..Thus, these results suggest that exposure to physiologically relevant doses of PB, DEET, and permethrin, alone or in combination, leads to neurobehavioral deficits and region-specific alterations in AChE and acetylcholine receptors...
  11. ncbi request reprint In utero exposure to nicotine and chlorpyrifos alone, and in combination produces persistent sensorimotor deficits and Purkinje neuron loss in the cerebellum of adult offspring rats
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 80:620-31. 2006
    ..Collectively, this study demonstrates that maternal exposure to environmental neurotoxic chemicals, i.e., nicotine and chlorpyrifos leads to developmental abnormalities in the offspring that persist latter into adulthood...
  12. ncbi request reprint Interaction of pyridostigmine bromide and N,N-diethyl-m-toluamide alone and in combination with P-glycoprotein expressed in Escherichia coli leaky mutant
    Eman M El-Masry
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 69:919-33. 2006
    ..This study improves our understanding of the basis of chemical interactions with DEET by defining the ability of drugs to interact with P-gp either as inhibitors or substrates, which may in turn lead to altered efficacy or toxicity...
  13. ncbi request reprint Maternal exposure of rats to nicotine via infusion during gestation produces neurobehavioral deficits and elevated expression of glial fibrillary acidic protein in the cerebellum and CA1 subfield in the offspring at puberty
    Ali Abdel-Rahman
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Toxicology 209:245-61. 2005
    ..These neurobehavioral and pathological deficits indicate that maternal nicotine exposure may produce long-term adverse health effects in the offspring...
  14. ncbi request reprint Imidacloprid induces neurobehavioral deficits and increases expression of glial fibrillary acidic protein in the motor cortex and hippocampus in offspring rats following in utero exposure
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 71:119-30. 2008
    ..These changes may have long-term adverse health effects in the offspring...
  15. ncbi request reprint Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats
    Ali Abdel-Rahman
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    J Toxicol Environ Health A 67:331-56. 2004
    ....
  16. ncbi request reprint Maternal exposure to nicotine and chlorpyrifos, alone and in combination, leads to persistently elevated expression of glial fibrillary acidic protein in the cerebellum of the offspring in late puberty
    Ali Abdel-Rahman
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 78:467-76. 2004
    ..Also, nicotine caused a decrease in the surviving neurons and an increased expression of GFAP in cerebellar white matter of the offspring on PND 60. These changes can lead to long-term neurological adverse health effects later in life...
  17. doi request reprint DFP initiated early alterations of PKA/p-CREB pathway and differential persistence of beta-tubulin subtypes in the CNS of hens contributes to OPIDN
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Toxicol Appl Pharmacol 240:132-42. 2009
    ....
  18. ncbi request reprint Early differential elevation and persistence of phosphorylated cAMP-response element binding protein (p-CREB) in the central nervous system of hens treated with diisopropyl phosphorofluoridate, an OPIDN-causing compound
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27708, USA
    Neurochem Res 27:183-93. 2002
    ....
  19. ncbi request reprint Sarin causes altered time course of mRNA expression of alpha tubulin in the central nervous system of rats
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27708, USA
    Neurochem Res 27:177-81. 2002
    ..Immediate induction and persistence of alpha tubulin transcripts in sarin-treated CNS suggest that sarin-induced neurotoxicity is in part mediated by the altered expression of cytoskeletal genes which may be regulated at multiple levels...
  20. ncbi request reprint Sarin (nerve agent GB)-induced differential expression of mRNA coding for the acetylcholinesterase gene in the rat central nervous system
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, PO Box 3813, Durham, NC 27708, USA
    Biochem Pharmacol 65:2041-7. 2003
    ....
  21. ncbi request reprint Binding of pyridostigmine bromide, N,N-diethyl-m-toluamide and permethrin, alone and in combinations, to human serum albumin
    Aqel W Abu-Qare
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 76:203-8. 2002
    ..These results showed that PB is highly bound to albumin protein, while the competition between PB, DEET and permethrin on binding sites of HSA as a possible site of interaction following combined administration in vivo is not likely...
  22. ncbi request reprint Toxicogenomic studies of the rat brain at an early time point following acute sarin exposure
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, P O Box 3813, Durham, NC, 27710, USA
    Neurochem Res 31:367-81. 2006
    ..Our model (based on current and previous studies) indicates that both degenerative and regenerative pathways are activated early and contribute to the level of neurodegeneration at a later time, leading to neuro-pathological alterations...
  23. ncbi request reprint Inhibition and recovery of maternal and fetal cholinesterase enzymes following a single oral dose of chlorpyrifos in rats
    Khaled M Ashry
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 76:30-9. 2002
    ..The rapid recovery of cholinesterase enzymes in the fetus is attributed to the de novo synthesis of AChE enzymes in the fetus compared to the mother...
  24. ncbi request reprint Gene expression profiles of the rat brain both immediately and 3 months following acute sarin exposure
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    Biochem Pharmacol 71:497-520. 2006
    ..Our model also predicts that besides dose and duration of post-treatment period, age and possibly other factors may be playing important roles in the regulation of pathways, leading to the neurotoxicity...
  25. ncbi request reprint Methyl parathion: a review of health effects
    Stephanie J Garcia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health B Crit Rev 6:185-210. 2003
    ..This review examines the well-documented neurotoxicity of methyl parathion as well as effects on other organ systems...
  26. ncbi request reprint Pharmacokinetic profile and placental transfer of a single intravenous injection of [(14)C]chlorpyrifos in pregnant rats
    Ali A Abdel-Rahman
    Department of Pharmacology and Cancer Biology, Box 3813, Duke University Medical Center, Durham, NC 27710, USA
    Arch Toxicol 76:452-9. 2002
    ..chlorpyrifos and its metabolites are distributed to all maternal and fetal tissues and plasma; and (3). the elimination of chlorpyrifos and TCP is slow, with redistribution from lipid stores a likely determinant of elimination rates...
  27. doi request reprint Autoantibodies to nervous system-specific proteins are elevated in sera of flight crew members: biomarkers for nervous system injury
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health A 76:363-80. 2013
    ..Thus, increased circulating serum autoantibodies resulting from neuronal damage may be used as biomarkers for chemical-induced CNS injury...
  28. ncbi request reprint Combined exposure to DEET (N,N-diethyl-m-toluamide) and permethrin: pharmacokinetics and toxicological effects
    Aqel W Abu-Qare
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    J Toxicol Environ Health B Crit Rev 6:41-53. 2003
    ....
  29. ncbi request reprint Organophosphorus ester-induced chronic neurotoxicity
    Mohamed B Abou-Donia
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Arch Environ Health 58:484-97. 2003
    ....
  30. ncbi request reprint Differential alteration of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA in the central nervous system of hens treated with diisopropylphosphorofluoridate (DFP)
    Tirupapuliyur V Damodaran
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, P O Box 3813, Durham, NC 27708, USA
    Neurochem Int 40:371-9. 2002
    ....
  31. ncbi request reprint A role for P-glycoprotein in environmental toxicology
    Aqel W Abu-Qare
    Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Toxicol Environ Health B Crit Rev 6:279-88. 2003
    ..Recent reports from the pharmaceutical studies on the significance of P-gp as transporters in altering the efficacy and toxicity clearly highlight the need for further research in interaction with environmental toxicants...
  32. ncbi request reprint Disruption of the blood-brain barrier and neuronal cell death in cingulate cortex, dentate gyrus, thalamus, and hypothalamus in a rat model of Gulf-War syndrome
    Ali Abdel-Rahman
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Caroloina 277109, USA
    Neurobiol Dis 10:306-26. 2002
    ..The various neurological symptoms reported by Gulf-War veterans could be linked to this kind of brain injury incurred during the war...
  33. ncbi request reprint Depleted uranium--the growing concern
    Aqel W Abu-Qare
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    J Appl Toxicol 22:149-52. 2002
    ..The use of depleted uranium during the Gulf and Kosovo Wars and the crash of a Boeing airplane carrying depleted uranium in Amsterdam in 1992 were implicated in a health concern related to exposure to depleted uranium...
  34. ncbi request reprint Reversal of P-glycoprotein expressed in Escherichia coli leaky mutant by ascorbic acid
    Eman M El-Masry
    Department of Pharmacology, Duke University Medical Center, Box 3813, Durham, NC 27710, USA
    Life Sci 73:981-91. 2003
    ..This study provide a heterologous system for mdr1 expression in E. coli leaky mutant that can be used as a system for the screening of P-gp inducers and inhibitors, since it is quick and simple...
  35. ncbi request reprint Protein levels of neurofilament subunits in the hen central nervous system following prevention and potentiation of diisopropyl phosphorofluoridate (DFP)-induced delayed neurotoxicity(1)
    Keqin Xie
    Neurotoxicology Laboratory, School of Life Science, University of Science and Technology of China, 230027, Hefei, Anhui, P R China
    Biochem Pharmacol 63:11-9. 2002
    ..However, results from PMSF post-treated hen spinal cords suggested that potentiation of OPIDN by PMSF was mediated by a mechanism different from that followed by DFP alone to produce OPIDN...