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Paraoxon: An Anticholinesterase That Triggers an Excitotoxic Cascade of Oxidative Stress, Adhesion Responses, and Synaptic Compromise
- Source :
- European Scientific Journal.
- Publication Year :
- 2017
- Publisher :
- European Scientific Institute, ESI, 2017.
-
Abstract
- The anticholinesterase paraoxon (Pxn) is an organophosphate (OP) and the active metabolite of the insecticide parathion. It potently inhibits the enzyme acetylcholinesterase and leads to enhanced glutamate release, diminished GABA uptake, oxidative damage, and neurodegeneration. The resulting increased levels of acetylcholine can trigger seizures and cause neuronal and excitotoxic damage in the brain. The brain susceptibility related to anticholinesterase toxins extends beyond potential brain damage and death from toxic levels of the agent. Asymptomatic low-level exposure to such toxins can also leave the brain vulnerable or even cause it to exhibit neurological problems later in life. The actions of Pxn and similar neurotoxins have been studied in order to examine the events associated with anticholinesterase toxicity in the brain. A recent study demonstrated that Pxn exposure initiates a pathogenic cascade involving seizure events and subsequent signs of damage including unique presynaptic vulnerability and associated behavioral deficits. In addition, Pxn-mediated synaptotoxicity is also associated with enhanced production of oxidative stress as well as integrin adhesion responses. These findings provide a better understanding of the molecular events involved in Pxn toxicity.
- Subjects :
- 0301 basic medicine
Paraoxon
Chemistry
Neurodegeneration
Glutamate receptor
Neurotoxicity
Excitotoxicity
Brain damage
Pharmacology
medicine.disease
medicine.disease_cause
Acetylcholinesterase
Article
03 medical and health sciences
chemistry.chemical_compound
030104 developmental biology
0302 clinical medicine
medicine
medicine.symptom
030217 neurology & neurosurgery
Oxidative stress
medicine.drug
Subjects
Details
- ISSN :
- 18577431 and 18577881
- Database :
- OpenAIRE
- Journal :
- European Scientific Journal
- Accession number :
- edsair.doi.dedup.....5d86bb54788189f6b45fdd3e26e54cd0