NDLI: Evidence that mouse brain neuropathy target esterase is a lysophospholipase.

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Evidence that mouse brain neuropathy target esterase is a lysophospholipase.

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Evidence that mouse brain neuropathy target esterase is a lysophospholipase.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Winrow, Christopher J. Barlow, Carrolee Sparks, Susan E. Casida, John E. Quistad, Gary B.
Description	Author Affiliation: Quistad GB ( Environmental Chemistry and Toxicology Laboratory, Department of Environmental Science, Policy, and Management, University of California, Berkeley, CA 94720-3112, USA.);
Abstract	Neuropathy target esterase (NTE) is inhibited by several organophosphorus (OP) pesticides, chemical warfare agents, lubricants, and plasticizers, leading to OP-induced delayed neuropathy in people (>30,000 cases of human paralysis) and hens (the best animal model for this demyelinating disease). The active site region of NTE as a recombinant protein preferentially hydrolyzes lysolecithin, suggesting that this enzyme may be a type of lysophospholipase (LysoPLA) with lysolecithin as its physiological substrate. This hypothesis is tested here in mouse brain by replacing the phenyl valerate substrate of the standard NTE assay with lysolecithin for an 'NTE-LysoPLA' assay with four important findings. First, NTE-LysoPLA activity, as the NTE activity, is 41-45% lower in Nte-haploinsufficient transgenic mice than in their wild-type littermates. Second, the potency of six delayed neurotoxicants or toxicants as in vitro inhibitors varies from IC50 0.02 to 13,000 nM and is essentially the same for NTE-LysoPLA and NTE (r2 = 0.98). Third, the same six delayed toxicants administered i.p. to mice at multiple doses inhibit brain NTE-LysoPLA and NTE to the same extent (r2 = 0.90). Finally, their in vivo inhibition of brain NTE-LysoPLA generally correlates with delayed toxicity. Therefore, OP-induced delayed toxicity in mice, and possibly the hyperactivity associated with NTE deficiency, may be due to NTE-LysoPLA inhibition, leading to localized accumulation of lysolecithin, a known demyelinating agent and receptor-mediated signal transducer. This mouse model has some features in common with OP-induced delayed neuropathy in hens and people but differs in the neuropathological signs and apparently the requirement for NTE aging.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	13
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Brain Enzymology Carboxylic Ester Hydrolases Physiology Lysophospholipase Animals Metabolism Chemistry Demyelinating Diseases Dose-Response Relationship, Drug Inhibitory Concentration 50 Lysophosphatidylcholines Mice Mice, Transgenic Models, Chemical Nervous System Diseases Chemically Induced Organophosphorus Compounds Adverse Effects Pesticides Recombinant Proteins Signal Transduction Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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