Phenol, 4-((4-(phenylmethoxy)phenyl)sulfonyl)-
Associated AOPs with Level of Relevance - 1 AOPs with at least 1 KE associated with chemical, where the KE(s) are neither MIE nor AO
| AOP Identifier |
AOP Title |
AO Classification |
OECD Status |
Taxonomic applicability |
Coverage Score
ⓘ
The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints.
|
KE Identifier |
KE Name |
| AOP:27 | Cholestatic Liver Injury induced by Inhibition of the Bile Salt Export Pump (ABCB11) | Gastrointestinal system disease | Under Development | Humans | 0.12 | KE:288 | Activation of specific nuclear receptors, Transcriptional change |
| AOP:439 | Activation of the AhR leading to metastatic breast cancer | Thoracic disease; Cancer | Under Development | Humans, Mice | 0.11 | KE:1971 | Increased, tumor growth |
| AOP:510 | Demethylation of PPAR promotor leading to vascular disrupting effects | Cardiovascular system disease | - | Human, Mouse, Zebrafish | 0.1 | KE:2165 | Activation of PPAR |
Associated AOPs with Level of Relevance - 2 AOPs with at least 1 AO associated with chemical, and no associated MIE
| AOP Identifier |
AOP Title |
AO Classification |
OECD Status |
Taxonomic applicability |
Coverage Score
ⓘ
The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints.
|
KE Identifier |
KE Name |
| AOP:139 | Alkylation of DNA leading to cancer 1 | Cancer | - | Homo sapiens, Mus musculus | 0.25 | KE:885 | Increase, Cancer |
| AOP:474 | Succinate dehydrogenase inactivation leads to cancer by promoting EMT | Cancer | Under Development | Human and other cells in culture | 0.2 | KE:885 | Increase, Cancer |
| AOP:505 | Reactive Oxygen Species (ROS) formation leads to cancer via inflammation pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:885 | Increase, Cancer |
| AOP:513 | Reactive Oxygen (ROS) formation leads to cancer via Peroxisome proliferation-activated receptor (PPAR) pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:885 | Increase, Cancer |
| AOP:534 | Succinate dehydrogenase (SDH) inhibition leads to cancer through oxidative stress | Cancer | - | Vertebrates | 0.17 | KE:885 | Increase, Cancer |
| AOP:546 | Succinate dehydrogenase inactivation leads to cancer through hypoxic-like mechanisms | Cancer | - | Human and other cells in culture | 0.2 | KE:885 | Increase, Cancer |
Associated AOPs with Level of Relevance - 3 AOPs with at least 1 MIE associated with chemical, and no associated AO
| AOP Identifier |
AOP Title |
AO Classification |
OECD Status |
Taxonomic applicability |
Coverage Score
ⓘ
The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints.
|
KE Identifier |
KE Name |
| AOP:232 | NFE2/Nrf2 repression to steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | | 0.12 | KE:1417 | NFE2/Nrf2 repression |
| AOP:507 | Nrf2 inhibition leading to vascular disrupting effects via inflammation pathway | Cardiovascular system disease | - | Mouse, Zebrafish, Human | 0.17 | KE:1417 | NFE2/Nrf2 repression |
| AOP:508 | Nrf2 inhibition leading to vascular disrupting effects through activating HIF1α, Semaphorin 6A, and Dll4-Notch pathway | Cardiovascular system disease | - | Mouse, Zebrafish, Human | 0.14 | KE:1417 | NFE2/Nrf2 repression |
| AOP:509 | Nrf2 inhibition leading to vascular disrupting effects through activating apoptosis signal pathway and mitochondrial dysfunction | Cardiovascular system disease | - | | 0.14 | KE:1417 | NFE2/Nrf2 repression |
No associated AOPs with Level of Relevance 5
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We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.