Journal
COUNTERMEASURES AGAINST CHEMICAL THREATS II
Volume 1378, Issue -, Pages 17-24Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.13115
Keywords
oxidative stress; organophosphates; acetylcholinesterase; nerve agents; reactive oxygen species
Funding
- NINDS NIH HHS [R01 NS086423, R01 NS039587, U01 NS083422, F31 NS086405, R21 NS072099] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS039587, R01NS086423, U01NS083422, R21NS072099, F31NS086405] Funding Source: NIH RePORTER
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Organophosphate (OP) nerve agents exert their toxicity through inhibition of acetylcholinesterase. The excessive stimulation of cholinergic receptors rapidly causes neuronal damage, seizures, death, and long-term neurological impairment in those that survive. Owing to the lethality of organophosphorus agents and the growing risk they pose, medical interventions that prevent OP toxicity and the delayed injury response are much needed. Studies have shown that oxidative stress occurs in models of subacute, acute, and chronic exposure to OP agents. Key findings of these studies include alterations in mitochondrial function and increased free radical-mediated injury, such as lipid peroxidation. This review focuses on the role of reactive oxygen species in OP neurotoxicity and its dependence on seizure activity. Understanding the sources, mechanisms, and pathological consequences of OP-induced oxidative stress can lead to the development of rational therapies for treating toxic exposures.
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