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Toxics
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Organophosphate-Induced Neurotoxicity: Countermeasures, Mechanisms, and Physiology
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Organophosphate-Induced Neurotoxicity: Countermeasures, Mechanisms, and Physiology

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Neurotoxicity".

Deadline for manuscript submissions: closed (16 March 2024) | Viewed by 8455

Special Issue Editor

Dr. Jeremy W. Chambers

E-Mail Website
Guest Editor
Biomolecular Sciences Institute, Florida International University, Miami, FL 33199, USA
Interests: neurodegeneration; organophosphates; neurotoxicity; drug discovery; protein kinases; protein-protein interactions

Special Issue Information

Dear Colleagues,

Organophosphates (OPs) are comprised of diverse compounds that include commonly used pesticides, fire retardants, industrial chemicals, and chemical weapon. Acute and chronic exposures to OPs can elicit immediate, intermediate, and chronic effects on the nervous system, including potentially contibuting to the onset of neurodegenerative disorders. While the primary mechanism of OP neurotoxicity has been canonically ascribed to inhibition of acetylcholinesterase, evidence is emerging that noncholinergic mechanisms may contibute to the neurotoxic effects following OP exposure. A variety of biochemical, cellular, and physiological manifestations have been detected following OP exposures in preclinical models and in affected patients, These include calcium dyshomeostasis, oxidative stress, neuroinflammation, excitotoxicity. As our knowledge of the mechanisms of OP neurotoxicity evolves, the prospects of identifying vaible therapeutic approaches to mitigate these effects and improve long-term diagnostic and prognostic capabilities increase. Consequently, the goals of this special issue is to assemble a body a literature to coordinate the rapidly growing and diversifying research surrounding OP-induced neuropathology and the concurrent mechanisms of neurotoxicity and to encourage the investigation of potential countermeasures in reproducible models of OP-induced dysfunction in the central and peripheral nervous system. Collectively, the special issue will be a platform to organize findings and guide the future research as a community.

Dr. Jeremy W. Chambers
Guest Editor

Manuscript Submission Information

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Keywords

  • organophosphate
  • neurotoxicity
  • countermeasures
  • excitotoxicity
  • oxidative stress
  • neuroinflammation
  • acetylcholinesterase
  • cholinergic signaling
  • calcium dyshomeostasis
  • neurodegeneration

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Published Papers (2 papers)

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Research

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24 pages, 4443 KiB  
Article
The α4 Nicotinic Acetylcholine Receptor Is Necessary for the Initiation of Organophosphate-Induced Neuronal Hyperexcitability
by Peter M. Andrew, Wei Feng, Jonas J. Calsbeek, Shane P. Antrobus, Gennady A. Cherednychenko, Jeremy A. MacMahon, Pedro N. Bernardino, Xiuzhen Liu, Danielle J. Harvey, Pamela J. Lein and Isaac N. Pessah
Toxics 2024, 12(4), 263; https://doi.org/10.3390/toxics12040263 - 31 Mar 2024
Viewed by 1214
Abstract
Acute intoxication with organophosphorus (OP) cholinesterase inhibitors can produce seizures that rapidly progress to life-threatening status epilepticus. Significant research effort has been focused on investigating the involvement of muscarinic acetylcholine receptors (mAChRs) in OP-induced seizure activity. In contrast, there has been far less [...] Read more.
Acute intoxication with organophosphorus (OP) cholinesterase inhibitors can produce seizures that rapidly progress to life-threatening status epilepticus. Significant research effort has been focused on investigating the involvement of muscarinic acetylcholine receptors (mAChRs) in OP-induced seizure activity. In contrast, there has been far less attention on nicotinic AChRs (nAChRs) in this context. Here, we address this data gap using a combination of in vitro and in vivo models. Pharmacological antagonism and genetic deletion of α4, but not α7, nAChR subunits prevented or significantly attenuated OP-induced electrical spike activity in acute hippocampal slices and seizure activity in mice, indicating that α4 nAChR activation is necessary for neuronal hyperexcitability triggered by acute OP exposures. These findings not only suggest that therapeutic strategies for inhibiting the α4 nAChR subunit warrant further investigation as prophylactic and immediate treatments for acute OP-induced seizures, but also provide mechanistic insight into the role of the nicotinic cholinergic system in seizure generation. Full article
(This article belongs to the Special Issue Organophosphate-Induced Neurotoxicity: Countermeasures, Mechanisms, and Physiology)
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Review

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15 pages, 1479 KiB  
Review
Mechanisms of Organophosphate Toxicity and the Role of Acetylcholinesterase Inhibition
by Vassiliki Aroniadou-Anderjaska, Taiza H. Figueiredo, Marcio de Araujo Furtado, Volodymyr I. Pidoplichko and Maria F. M. Braga
Toxics 2023, 11(10), 866; https://doi.org/10.3390/toxics11100866 - 18 Oct 2023
Cited by 10 | Viewed by 6366
Abstract
Organophosphorus compounds (OPs) have applications in agriculture (e.g., pesticides), industry (e.g., flame retardants), and chemical warfare (nerve agents). In high doses or chronic exposure, they can be toxic or lethal. The primary mechanism, common among all OPs, that initiates their toxic effects is [...] Read more.
Organophosphorus compounds (OPs) have applications in agriculture (e.g., pesticides), industry (e.g., flame retardants), and chemical warfare (nerve agents). In high doses or chronic exposure, they can be toxic or lethal. The primary mechanism, common among all OPs, that initiates their toxic effects is the inhibition of acetylcholinesterase. In acute OP exposure, the subsequent surge of acetylcholine in cholinergic synapses causes a peripheral cholinergic crisis and status epilepticus (SE), either of which can lead to death. If death is averted without effective seizure control, long-term brain damage ensues. This review describes the mechanisms by which elevated acetylcholine can cause respiratory failure and trigger SE; the role of the amygdala in seizure initiation; the role of M1 muscarinic receptors in the early stages of SE; the neurotoxic pathways activated by SE (excitotoxicity/Ca++ overload/oxidative stress, neuroinflammation); and neurotoxic mechanisms linked to low-dose, chronic exposure (Ca++ dyshomeostasis/oxidative stress, inflammation), which do not depend on SE and do not necessarily involve acetylcholinesterase inhibition. The evidence so far indicates that brain damage from acute OP exposure is a direct result of SE, while the neurotoxic mechanisms activated by low-dose chronic exposure are independent of SE and may not be associated with acetylcholinesterase inhibition. Full article
(This article belongs to the Special Issue Organophosphate-Induced Neurotoxicity: Countermeasures, Mechanisms, and Physiology)
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