Portal:AOP/Mission
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(New page: The purpose of this portal is to create a collection of AOPs on the molecular level for the AOPs that are, or will be created for the [http://www.eu-toxrisk.eu/ EU-ToxRisk] program, in whi...) |
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* Inhibition of β-oxidation leads to liver steatosis | * Inhibition of β-oxidation leads to liver steatosis | ||
| - | * HDAC inhibition, folate antagonism | + | * HDAC inhibition, folate antagonism and oxidative stress lead to teratogenicity |
* Oxidative stress leads to hepatotoxicity | * Oxidative stress leads to hepatotoxicity | ||
* Oxidative stress leads to nephrotoxicity | * Oxidative stress leads to nephrotoxicity | ||
Revision as of 13:12, 6 April 2017
The purpose of this portal is to create a collection of AOPs on the molecular level for the AOPs that are, or will be created for the EU-ToxRisk program, in which Open PHACTS Foundation (OPF) is responsible for AOP creation. The subjects of the first AOPs are linked to the use cases of the EU-ToxRisk program, and there will be a team of experts involved in the creation of each AOP.
The proposed list of the first set of AOPs to be created:
- Inhibition of β-oxidation leads to liver steatosis
- HDAC inhibition, folate antagonism and oxidative stress lead to teratogenicity
- Oxidative stress leads to hepatotoxicity
- Oxidative stress leads to nephrotoxicity
- Disturbance of the respiratory chain leads to mitotoxicity
- PPAR activation leads to hepatoxicity
- OAT overactivation leads to nephrotoxicity
- PXR activation leads to liver steatosis
- NAPQI production causes hepatotoxicity
- MTP impairment leads to hepatotoxicity
- CYP51 inhibition causes embryotoxicity
- Epithelial damage leads to popcorn lung
Basic strategies and principles for general AOPs are described in this paper:
Villeneuve et al. (2014). Adverse Outcome Pathway (AOP) Development I: Strategies and Principles. Toxicological Sciences PubMed
