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
Key Event Relationship Description
Evidence Supporting this KER
- 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.
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 and 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.
Known modulating factors
Known Feedforward/Feedback loops influencing this KER
Domain of Applicability
This relationship is likely relevant to all organisms with a heart.