
This AOP is licensed under a Creative Commons Attribution 4.0 International License.
Aop: 265
Title
Uncoupling of oxidative phosphorylation leading to growth inhibition via decreased lipid storage
Short name
Graphical Representation
Point of Contact
Contributors
- You Song
- Cataia Ives
Status
Author status | OECD status | OECD project | SAAOP status |
---|---|---|---|
Under development: Not open for comment. Do not cite | Under Development | 1.92 | Included in OECD Work Plan |
This AOP was last modified on July 16, 2022 18:37
Revision dates for related pages
Page | Revision Date/Time |
---|---|
Decrease, Coupling of oxidative phosphorylation | May 28, 2021 07:59 |
Decrease, Growth | July 06, 2022 07:36 |
Decrease, Adenosine triphosphate pool | June 14, 2021 13:40 |
Increase, Fatty acid beta-oxidation | December 04, 2020 15:21 |
Decrease, Lipid storage | November 25, 2020 10:23 |
Decrease, Coupling of OXPHOS leads to Decrease, ATP pool | July 06, 2022 07:39 |
Decrease, ATP pool leads to Increase, Fatty acid β-oxidation | December 04, 2020 15:24 |
Increase, Fatty acid β-oxidation leads to Decrease, Lipid storage | December 04, 2020 15:24 |
Decrease, Lipid storage leads to Decrease, Growth | December 04, 2020 15:25 |
Abstract
The proposed project aims to develop a network of AOPs for mitochondrial uncoupler mediated adverse effects on aquatic organisms.
AOP Development Strategy
Context
The mitochondrion is central for diverse types of physiological processes, such as energy production, cell cycle regulation, lipid metabolism and ion homeostasis. Mitochondrial dysfunction has frequently been reported as a common (eco)toxicological effect induced by a wide range of environmental stressors through direct or indirect modes of action (Meyer et al., 2013). Chemical mediated mitochondrial dysfunctions are tightly associated with various diseases in human, such as neurodegeneration, cardiovascular malfunction, diabetes and cancer, and multiple types of effects in wildlife, such as metabolic disorders, growth arrest, developmental abnormalities, reproduction failure, mortality and population decline (Meyer et al., 2013). Several mitochondrial dysfunction related MIEs have been well characterized, such as uncoupling of oxidative phosphorylation (OXPHOS) and inhibition of specific protein complexes in the mitochondrial electron transport chain. These MIEs commonly affect the mitochondrial membrane potential and ATP synthetic processes, induce reactive oxygen species (ROS) and oxidative damage to DNA, protein and lipid, modulate plasma membrane ion transporter activities and trigger programmed cell death.
Strategy
Summary of the AOP
Events:
Molecular Initiating Events (MIE)
Key Events (KE)
Adverse Outcomes (AO)
Type | Event ID | Title | Short name |
---|
MIE | 1446 | Decrease, Coupling of oxidative phosphorylation | Decrease, Coupling of OXPHOS |
KE | 1771 | Decrease, Adenosine triphosphate pool | Decrease, ATP pool |
KE | 1312 | Increase, Fatty acid beta-oxidation | Increase, Fatty acid β-oxidation |
KE | 1823 | Decrease, Lipid storage | Decrease, Lipid storage |
AO | 1521 | Decrease, Growth | Decrease, Growth |
Relationships Between Two Key Events (Including MIEs and AOs)
Title | Adjacency | Evidence | Quantitative Understanding |
---|
Network View
Prototypical Stressors
Life Stage Applicability
Life stage | Evidence |
---|---|
Not Otherwise Specified | |
All life stages | Not Specified |
Taxonomic Applicability
Sex Applicability
Sex | Evidence |
---|---|
Unspecific | Not Specified |