| 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:18 | PPARα activation in utero leading to impaired fertility in males | Reproductive system disease | Under Review | Human, Rat, Mouse | 0.12 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:41 | Sustained AhR Activation leading to Rodent Liver Tumours | Cancer; Gastrointestinal system disease | Under Review | Rattus sp. ABTC 42503, Mus sp. 2000082 | 0.2 | KE:139 | N/A, Hepatotoxicity, Hepatopathy, including a constellation of observable effects |
| AOP:64 | Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male Fertility | Reproductive system disease | - | Rattus norvegicus | 0.14 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:112 | Increased dopaminergic activity leading to endometrial adenocarcinomas (in Wistar rat) | Reproductive system disease; Cancer | - | Rattus norvegicus | 0.17 | KE:749 | Decreased, Progesterone from corpus luteum |
| AOP:120 | Inhibition of 5α-reductase leading to Leydig cell tumors (in rat) | Cancer; Reproductive system disease | - | Rattus norvegicus, Mus musculus | 0.2 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:124 | HMG-CoA reductase inhibition leading to decreased fertility | Reproductive system disease | - | Rattus rattus | 0.17 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:288 | Inhibition of 17α-hydrolase/C 10,20-lyase (Cyp17A1) activity leads to birth reproductive defects (cryptorchidism) in male (mammals) | Endocrine system disease | - | Human, Rat | 0.12 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:309 | Luteinizing hormone receptor antagonism leading to reproductive dysfunction | Unclassified | - | Fish | 0.29 | KE:1693 | Reduction, Plasma progesterone concentration |
| KE:1692 | Reduction, Progesterone synthesis | ||||||
| AOP:447 | Kidney failure induced by inhibition of mitochondrial electron transfer chain through apoptosis, inflammation and oxidative stress pathways | Urinary system disease | - | 0.08 | KE:1097 | Occurrence, renal proximal tubular necrosis | |
| AOP:472 | DNA adduct formation leading to kidney failure | Urinary system disease | - | 0.11 | KE:1097 | Occurrence, renal proximal tubular necrosis | |
| AOP:496 | Androgen receptor agonism leading to reproduction dysfunction (in zebrafish) | Unclassified | - | Zebrafish | 0.1 | KE:1690 | Decrease, circulating testosterone levels |
| 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:220 | Cyp2E1 Activation Leading to Liver Cancer | Cancer; Gastrointestinal system disease | WPHA/WNT Endorsed | Rodents, Homo sapiens | 0.4 | KE:1395 | Liver Cancer |
| KE:1393 | Hepatocytotoxicity | ||||||
| AOP:304 | TBX1 inhibition leading to congenital cardiac conotruncal anomalies | Cardiovascular system disease | - | 0.17 | KE:1685 | Anomalies, Congenital cardiac conotruncal | |
| AOP:463 | The AOP framwork on silica nanopariticles induced hepatoxicity | Gastrointestinal system disease | - | 0.09 | KE:2034 | liver dysfunction |
| 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:118 | Chronic cytotoxicity leading to hepatocellular adenomas and carcinomas (in mouse and rat) | Cancer; Gastrointestinal system disease | - | Mus musculus, Rattus norvegicus | 0.25 | KE:786 | Increase, Cytotoxicity (hepatocytes) |
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.