TITLE

Lessons for neurotoxicology from selected model compounds: SGOMSEC joint report

AUTHOR(S)
Rice, Deborah C.; de Duffard, Ana Maria Evang
PUB. DATE
April 1996
SOURCE
Environmental Health Perspectives Supplements;Apr96 Supplement 2, Vol. 104, p205
SOURCE TYPE
Periodical
DOC. TYPE
Article
ABSTRACT
Discusses the lessons for neurotoxicology that may be learned from intensive investigation of selected neurotoxic agents. Characterization of the agents' effects on human population; Predicted ability of standard neurotoxicity tests to detect neurotoxicity; Congruence of exposure levels at which neurotoxicity is observed in animals and humans.
ACCESSION #
9605234806

 

Related Articles

  • Neurotoxicity risk assessment of MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine) as a synthetic impurity of drugs. Juergen Kramer, P.; Caldwell, J.; Hofmann, A.; Tempel, P.; Weisse, G. // Human & Experimental Toxicology;1998, Vol. 17 Issue 5, p283 

    1-Methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) induces symptoms indistinguishable from those of Parkinson's disease. It selectively destroys dopaminergic neurons in the substantia nigra and the globus pallidus. Death of these same neurons is apparently the cause of idiopathic Parkinson's...

  • Risk assessment for neurobehavioral toxicity: SGOMSEC joint report. Hattis, Dale; Glowa, John // Environmental Health Perspectives Supplements;Apr96 Supplement 2, Vol. 104, p217 

    Focuses on the development of the behavioral end points of neurotoxicity risk assessment from simple qualitative guidelines to quantitative models. Emergence of neurobehavioral toxicology as an issue of concern; Effectiveness and limits of risk assessment methodologies; Advantages and...

  • 3-Mercaptopyruvate sulfurtransferase is expressed in medulla oblongata and can be up-regulated by intrauterine cigarette exposure in neonatal rats. Nie, L.; Hu, Y.; Yan, X.; Li, M.; Chen, L.; An, H.; Zhou, H.; Zheng, Y. // Proceedings of the Physiological Society;2013, p638P 

    Noxious substances released from burning cigarettes may cause hypoxia and neurotoxic effects that impede the development of the central nervous system, including brainstem. Our previous studies demonstrated that endogenous hydrogen sulphide (H2S) participate in regulation of respiration (Hu et...

  • Increased Neurotoxicity Following Concurrent Exposure to Pyridostigmine Bromide, DEET, and Chlorpyrifos. ABOU-DONIA, MOHAMED B.; WILMARTH, KENNETH R.; ABDEL-RAHMAN, ALI A.; JENSEN, KARL F.; OEHME, FREDERICK W.; KURT, THOMAS L. // Fundamental & Applied Toxicology;1996, Vol. 34 Issue 2, p201 

    The operating environment of the service personnel during the Persian Gulf War involved psychological, biological, and chemical elements including exposure to pesticides such as the insect repellent DEET (N,N-diethyl-m-toluamide) and the insecticide chlorpyrifos (O,O-diethyl...

  • Development of a High-Throughput Screening Assay for Chemical Effects on Proliferation and Viability of Immortalized Human Neural Progenitor Cells. Joseph M. Breier; Nicholas M. Radio; William R. Mundy; Timothy J. Shafer // Toxicological Sciences;Sep2008, Vol. 105 Issue 1, p119 

    There is considerable public concern that the majority of commercial chemicals have not been evaluated for their potential to cause developmental neurotoxicity. Although several chemicals are assessed annually under the current developmental neurotoxicity guidelines, time, resource, and animal...

  • Normal glucose enhances neuronal regeneration after lidocaine-induced injury. Nazeer, A. Abdel; Saito, S.; Sayed, S.; Hassan, L.; Askar, F.; Al-jahdari, W.; Seki, T.; Hideaki, O. // BJA: The British Journal of Anaesthesia;Apr2010, Vol. 104 Issue 4, p482 

    Background: Local anaesthetics exhibit direct neurotoxic effects on neurones. Numerous studies have investigated the factors that may reverse this neuropathology, but the effects of glucose conditions on neuronal regeneration after lidocaine-induced injury have not been examined by observing...

  • Release of full-length PrPC from cultured neurons following neurotoxic challenges. Wang, Kevin K. W.; Zoltewicz, J. Susie; Chiu, Allen; Zhiqun Zhang; Rubenstein, Richard // Frontiers in Neurology;Oct2012, Vol. 3, p1 

    The susceptibility of the normal cellular prion protein isoform, cellular prion protein (PrPC), to proteolytic digestion has been well documented. In addition, a link between PrPC and the cytosolic protease, calpain, has been reported although the specifics of the interaction remain unclear.We...

  • BOX 7-2 TETANUS AND BOTULISM. Scanlon, Valerie C.; Sanders, Tina // Essentials of Anatomy & Physiology;Jan2007, p146 

    Information on tetanus and botulism from Chapter 7 of the book "Essentials of Anatomy & Physiology" is presented. Diseases are sometimes caused by the toxins produced by several bacteria. A definition of neurotoxin is presented. Tetanus refers to the inability of muscles to relax. One of the...

  • Neurotoxicity induces cleavage of p35 to p25 by calpain. Lee, Ming-sum; Kwon, Young T.; Li, Mingwei; Peng, Junmin; Friedlander, Robert M.; Tsai, Li-Huei // Nature;5/18/2000, Vol. 405 Issue 6784, p360 

    Reports on a study which shows that neurotoxicity induces cleavage of p35 to p25 by calpain. Neurite outgrowth and cortical lamination in the brain which require cyclin-dependent kinase 5 (cdk5) and its neuron-specific activator p35; Production of p25 by proteolytic cleavage of p35; Use of...

Share

Read the Article

Other Topics