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AOP: 26
Title
Calcium-mediated neuronal ROS production and energy imbalance
Short name
Graphical Representation
Point of Contact
Contributors
- Lyle Burgoon
- Erik Mylroie
- Brendan Ferreri-Hanberry
Coaches
OECD Information Table
OECD Project # | OECD Status | Reviewer's Reports | Journal-format Article | OECD iLibrary Published Version |
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This AOP was last modified on May 26, 2024 20:39
Revision dates for related pages
Page | Revision Date/Time |
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Inhibition, Ca++ ATPase | September 16, 2017 10:14 |
Increase, Ca++ (intracellular) | September 16, 2017 10:14 |
Disruption, Mitochondrial electron transport chain | September 16, 2017 10:14 |
Decrease, Mitochondrial ATP production | September 16, 2017 10:14 |
Increase, Reactive Oxygen Species production | April 11, 2021 18:03 |
Decreased, Nitric Oxide | September 16, 2017 10:14 |
Decreased, Long-term potentiation (LTP) | September 16, 2017 10:14 |
Increased, Oxidative damage | December 03, 2016 16:33 |
Inhibition, Ca++ ATPase leads to Increase, Ca++ (intracellular) | December 03, 2016 16:37 |
Increase, Ca++ (intracellular) leads to Disruption, Mitochondrial electron transport chain | December 03, 2016 16:37 |
Disruption, Mitochondrial electron transport chain leads to Decrease, Mitochondrial ATP production | December 03, 2016 16:37 |
Disruption, Mitochondrial electron transport chain leads to Increase, ROS production | December 03, 2016 16:37 |
Decreased, Nitric Oxide leads to Decreased, Long-term potentiation (LTP) | December 03, 2016 16:37 |
Increase, ROS production leads to Decreased, Nitric Oxide | December 03, 2016 16:37 |
Increase, ROS production leads to Increased, Oxidative damage | December 03, 2016 16:37 |
Abstract
Chemicals may lead to neurotoxicity through the inhibition of calcium ATPase activity, leading to increased intracellular calcium, increased ROS, and energy imbalance. This may lead to impaired nuerotransmission and oxidative neuronal damage.
AOP Development Strategy
Context
Strategy
Summary of the AOP
Events:
Molecular Initiating Events (MIE)
Key Events (KE)
Adverse Outcomes (AO)
Type | Event ID | Title | Short name |
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MIE | 51 | Inhibition, Ca++ ATPase | Inhibition, Ca++ ATPase |
KE | 50 | Increase, Ca++ (intracellular) | Increase, Ca++ (intracellular) |
KE | 178 | Disruption, Mitochondrial electron transport chain | Disruption, Mitochondrial electron transport chain |
KE | 40 | Decrease, Mitochondrial ATP production | Decrease, Mitochondrial ATP production |
KE | 257 | Increase, Reactive Oxygen Species production | Increase, ROS production |
KE | 193 | Decreased, Nitric Oxide | Decreased, Nitric Oxide |
KE | 166 | Decreased, Long-term potentiation (LTP) | Decreased, Long-term potentiation (LTP) |
AO | 356 | Increased, Oxidative damage | Increased, Oxidative damage |
Relationships Between Two Key Events (Including MIEs and AOs)
Title | Adjacency | Evidence | Quantitative Understanding |
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Network View
Prototypical Stressors
Life Stage Applicability
Taxonomic Applicability
Sex Applicability
Overall Assessment of the AOP
Consider the following criteria (may include references to KE Relationship pages): 1. concordance of dose-response relationships; 2. temporal concordance among the key events and adverse effect; 3. strength, consistency, and specificity of association of adverse effect and initiating event; 4. biological plausibility, coherence, and consistency of the experimental evidence; 5. alternative mechanisms that logically present themselves and the extent to which they may distract from the postulated AOP. It should be noted that alternative mechanisms of action, if supported, require a separate AOP; 6. uncertainties, inconsistencies and data gaps.