The Part Played by Inhibition of Cholinesterases of the CNS in Producing Paralysis in Chickens

Austin, L.; Davies, D. R.

doi:10.1111/j.1476-5381.1954.tb00833.x

Cited by 13 publications

(3 citation statements)

References 11 publications

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“…The enhancement of the central activity of an appropriate chemical by an anti-ChE compound may be another example of an incidental action, similar to the production of demyelinization by certain anti-ChE agents (SMITH and LILLIE 1931, PETRY 1951, BARNES and DENZ 1953, BIDSTRUP et al 1953, AUSTIN and DAVIES 1954, CAVANAUGH and THOMPSON 1954, DURHAM et al 1956, PETTY 1958see Chapter 19. As such, these actions may have no connection with the major mechanism of toxicity of the anti-ChE agents for the central nervous system, but may be significant factors in the prophylactic or therapeutic employment of other chemicals in poisoning by anti-ChE's.…”

Section: Stimulation and Depression Of Brain Stem And Cerebral Cmentioning

confidence: 96%

Pharmacological Antagonists of the Anticholinesterase Agents

Wills¹

1963

Cholinesterases and Anticholinesterase Agents

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Section: Stimulation and Depression Of Brain Stem And Cerebral Cmentioning

confidence: 96%

Pharmacological Antagonists of the Anticholinesterase Agents

Wills¹

1963

Cholinesterases and Anticholinesterase Agents

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“…Repeated small and large lethal subcutaneous doses of sarin failed to produce OPIDN (doses’ size and route of exposure were not specified) (Austin & Davies 1954). Administration of 26–28 daily LD 50 doses (25 μg/kg dose, i.m.)…”

Section: Incidences Of Opidnmentioning

confidence: 99%

Sarin (GB, O-isopropyl methylphosphonofluoridate) neurotoxicity: critical review

Abou‐Donia

Siracuse

Gupta

et al. 2016

Critical Reviews in Toxicology

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Sarin (GB, O-isopropyl methylphosphonofluoridate) is a potent organophosphorus (OP) nerve agent that inhibits acetylcholinesterase (AChE) irreversibly. The subsequent build-up of acetylcholine (ACh) in the central nervous system (CNS) provokes seizures and, at sufficient doses, centrally-mediated respiratory arrest. Accumulation of ACh at peripheral autonomic synapses leads to peripheral signs of intoxication and overstimulation of the muscarinic and nicotinic receptors, which is described as “cholinergic crisis” (i.e. diarrhea, sweating, salivation, miosis, bronchoconstriction). Exposure to high doses of sarin can result in tremors, seizures, and hypothermia. More seriously, build-up of ACh at neuromuscular junctions also can cause paralysis and ultimately peripherally-mediated respiratory arrest which can lead to death via respiratory failure. In addition to its primary action on the cholinergic system, sarin possesses other indirect effects. These involve the activation of several neurotransmitters including gamma-amino-butyric acid (GABA) and the alteration of other signaling systems such as ion channels, cell adhesion molecules, and inflammatory regulators. Sarin exposure is associated with symptoms of organophosphate-induced delayed neurotoxicity (OPIDN) and organophosphate-induced chronic neurotoxicity (OPICN). Moreover, sarin has been involved in toxic and immunotoxic effects as well as organophosphate-induced endocrine disruption (OPIED). The standard treatment for sarin-like nerve agent exposure is post-exposure injection of atropine, a muscarinic receptor antagonist, accompanied by an oxime, an AChE reactivator, and diazepam.

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“…The agents were given intramuscularly as a 1% dilution in 10% ethanol saline (Austin and Davies, 1954), within 0.5 hr. of preparation of the solution.…”

Section: Biological Methodsmentioning

confidence: 99%

The Relationship Between the Chemical Structure and Neurotoxicity of Alkyl Organophosphorus Compounds

Davies¹,

Holland²,

Rumens³

1960

British Journal of Pharmacology and Chemotherapy

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Thirty‐six alkyl organophosphorus compounds have been tested for neurotoxicity in the chicken. The individual compounds were chosen to enable the importance of each portion of the molecule to be assessed in relation to the property of neurotoxicity. Seventeen substances were found to be neurotoxic, fifteen for the first time. All of these contained fluorine. On the basis of the results reported, certain predictions have been made about the chemical structure of compounds which would be expected to be neurotoxic. The importance of fluorine suggests that it plays a direct role in the development of the biochemical lesion, and this may occur as the result of its being carried by the molecule as a whole to specific areas in the nervous system. By the action of cholinesterase, the P‐F bond may be ruptured and ionic fluorine liberated where it blocks some metabolic cycle.

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The Part Played by Inhibition of Cholinesterases of the CNS in Producing Paralysis in Chickens

Cited by 13 publications

References 11 publications

Pharmacological Antagonists of the Anticholinesterase Agents

Pharmacological Antagonists of the Anticholinesterase Agents

Sarin (GB, O-isopropyl methylphosphonofluoridate) neurotoxicity: critical review

The Relationship Between the Chemical Structure and Neurotoxicity of Alkyl Organophosphorus Compounds

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