| 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:453 | Reactive oxygen species and subsequent oxidative stress lead to increased incidence of digestive morbidity and mortality in the general population | Gastrointestinal system disease | - | 0.08 | KE:1995 | Abnormal lipid metabolism | |
| AOP:469 | Reactive oxygen speicies overproduction leading to increased digestive morbidity and mortality in generation population | Gastrointestinal system disease | - | 0.08 | KE:1995 | Abnormal lipid metabolism | |
| AOP:513 | Reactive Oxygen (ROS) formation leads to cancer via Peroxisome proliferation-activated receptor (PPAR) pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:1060 | Alteration, lipid metabolism |
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.