Organophosphorus-Induced Delayed Neuropathy

Ehrich, Marion; Jortner, Bernard S.

doi:10.1016/b978-0-12-374367-1.00069-0

Cited by 16 publications

(9 citation statements)

References 196 publications

(263 reference statements)

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“…Biochemical studies have shown that OPIDN agents inhibit a neuronal, nonspecific carboxylesterase termed neuropathy target esterase (NTE) (25,44). The specific relationship between organophosphate binding to NTE and subsequent neuropathy is not understood, but recent research has indicated that only organophosphates that cause aging of phosphorylated NTE cause OPIDN, and that aging of at least 70% of NTE is necessary (25).…”

Section: Organophosphate-induced Delayed Neuropathymentioning

confidence: 99%

“…Exposure to agents known to cause OPIDN (TOTP, DFP, mipafox, and leptophos) is associated with a Wallerian "dying back" degeneration of large-diameter axons and their myelinic sheaths in distal parts of the peripheral nerves and long spinal cord tracts. Bilateral degenerative change in distal axons and terminals resulting in breakdown of neuritic segments and myelin sheaths have been shown (25,44,45).…”

Section: Organophosphate-induced Delayed Neuropathymentioning

confidence: 99%

“…These symptoms can occur up to 2-3 weeks after a single exposure. Several recent reviews addressing OPIDN exist (25,44,45).…”

Section: Organophosphate-induced Delayed Neuropathymentioning

confidence: 99%

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Organophosphorus Pesticides

Storm¹

2012

Patty's Toxicology

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Most organophosphorus compounds today fall into two general groups: the so‐called nerve agents, that are very acutely toxic and organophosphorus pesticides that are less toxic. Nerve agents were generally the first toxic organophosphorus developed, and were the original basis for organophosphorus pesticides. Interest about nerve agents has increased lately given concerns about their potential use in terrorist acts. Organophosphate nerve agents and pesticides are a highly diverse group of chemicals. They are all characterized by their ability to inhibit the enzyme acetylcholinesterase (AChE) that deactivates the neurotransmitter acetylcholine (ACh). At present, the widest use of organophosphorus compounds is as pesticides, although they have also been used as therapeutic agents, gasoline additives, hydraulic fluids, cotton defoliants, fire retardants, plastic components, growth regulators, and industrial intermediates to a much smaller extent. Compounds in this class are numerous and have been categorized in many ways according to the nature of the substituents. Gallo and Lawryk (1991) [2], for example, categorized them into four main groups I–IV based on the characteristics of the leaving group (X). Group I compounds, phosphorylcholines, have a leaving group that contains a quaternary nitrogen and are among the most potent organophosphates (e.g., Shradan). Group II compounds, fluorophosphates, have a fluoride leaving group and are also generally highly toxic (e.g., diisopropyl fluorophosphate). Group III compounds have leaving groups that contain cyanide or a halogen other than fluoride and are generally less potent than group I or II (e.g., Parathion). Group IV contains most of the organophosphates used as insecticides today. These compounds have alkoxy, alkylthio, aryloxy, arylthio, or heterocyclic leaving groups and a wide variety of other substituents. Another classification scheme is based on the nature of the atoms that immediately surround the central phosphorus atom and results in 14 different categories. According to this scheme, phosphates are the prototype for the entire class and are those compounds where all four atoms that surround the phosphorus atom are oxygen (e.g., dichlorvos, mevinphos). Sulfur‐containing organophosphate compounds (phosphorothioates, phosphorothiolates, phosphorodithioates, and phosphorodithiolates) are far more numerous than phosphates and include well‐recognized organophosphate insecticides such as parathion, diazinon, chlorpyrifos, etc. Other groups contain nitrogen (phosphoramides and phosphorodiamides), nitrogen and sulfur (phosphoramidothionates and phosphoramidothiolates), carbon (phosphonates and phosphinates), or carbon and sulfur (phosphonothionates, phosphonothionothiolates, and phosphinothionates). All aspects of organophosphate chemistry, toxicity, analysis, and exposure potential have been previously and comprehensively reviewed. In addition, information regarding the toxicity of organophosphorus pesticides in particular has expanded greatly in recent years as a result of toxicity data supplied by registrants to the U.S. EPA's Office of Pesticides to support reregistration. These data have been made publicly available by the U.S. EPA on its Internet Web site ( www.epa.gov/pesticides ). The following discussion draws heavily from recent reviews and also includes summaries of relevant toxicity data submitted to, and made available by, the U.S. EPA.

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Section: Organophosphate-induced Delayed Neuropathymentioning

confidence: 99%

Section: Organophosphate-induced Delayed Neuropathymentioning

confidence: 99%

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Organophosphorus Pesticides

Storm¹

2012

Patty's Toxicology

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“…These include pro-toxicants (needing prior activation by liver microsomes to produce a toxic metabolite) such as leptophos and tri- ortho -tolyl phosphate (TOTP) and direct toxicants such as diisopropyl phosphorofluoridate, mipafox, and tolyl saligenin phosphate. Chemical features of these neurotoxicants include phosphorus in the pentavalent state, phosphorus with an oxygen attached by a coordinate covalent bond, and at least one oxygen or amine bridge linking an R group to phosphorus (Ehrich and Jortner 2010).…”

Section: Pathology Of Toxic Peripheral Neuropathymentioning

confidence: 99%

Common Structural Lesions of the Peripheral Nervous System

Jortner

2019

Toxicol Pathol

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This review illustrates common lesions of peripheral nerve myelinated fibers that occur in toxic neuropathy. These distinctive structural changes help to define the site of toxicant activity and thus predict the course of neurotoxic disease and recovery. Neuronopathy is the condition where the primary injury is directed to the neuronal cell body giving rise to a peripheral nerve axon. Axonopathy occurs when the axon is the primary target, and myelinopathy develops where the Schwann cell and/or myelin sheath is the primary target; these conditions can be discriminated early during the course of nerve fiber degeneration, but reciprocal influences between axon and myelin result in degeneration of both structures late in the disease.

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“…There also is molecular rearrangement of the inhibited enzyme, termed aging. A degree of inhibition of 70% or more after a single dose will result in axonopathy progressing to myelinated fiber breakdown some 7-10 days after dosing in the chicken, a standard test animal for this neuropathy (Figures 9, 10, and 11) (Ehrich and Jortner 2010). This process preferentially affects larger fibers, and again it is more prominent distally.…”

Section: Toxin-induced Pathologic Reactions Of Peripheral Nervesmentioning

confidence: 99%