Inhibition, Acetylcholinesterase (AchE) leads to Induction, Ataxia, paralysis, or hyperactivity
Upstream eventInhibition, Acetylcholinesterase (AchE)
Induction, Ataxia, paralysis, or hyperactivity
Key Event Relationship Overview
AOPs Referencing Relationship
Life Stage Applicability
How Does This Key Event Relationship Work
Weight of Evidence
- Given the role of acetycholinesterase in degrading acetylcholine and the importance of acetycholine regulating contraction of skeletal muscle via (N2, Nm) nicotinic acetylcholine receptors, there is a well established plausible connection between acetylcholinesterase inhibition and ataxia and/or paralysis.
Empirical Support for Linkage
Include consideration of temporal concordance here
- A study of profenofos in earthworms (Eisenis foetida) found direct correlations of physiological impacts (e.g., disintegration of circular and longitudinal muscles, bloody lesion, ruptures of the body) and AChE inhibition (Chakra Reddy and Rao 2008).
- Within one hour of exposure of broiler chicks to dichlorvos or diazinon symptoms indicative of cholinergic poisoning were observed including respiratory difficulty (gasping), tremors and convulsions (Al-Zubaidy et al. 2011).
- AChE was inhibited from 81.5-92% in the brain of kestrels from day 1 to day 3 of a fenthion exposure, resulting in symptoms typical of AChE poisoning (e.g., paralysis, salivation, tremors, mortality), with a concurrent decrease in the amount of prey consumed (Hunt et al., 1991).
Uncertainties or Inconsistencies
Quantitative Understanding of the Linkage
- Because this linkage is indirect, the quantitative understanding of this relationship was not evaluated. There may be data upon which to develop a correlation-based relationship.
Evidence Supporting Taxonomic Applicability
This relationship is likely relevant to all organisms with a heart.