| 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:112 | Increased dopaminergic activity leading to endometrial adenocarcinomas (in Wistar rat) | Reproductive system disease; Cancer | - | Rattus norvegicus | 0.17 | KE:111 | Agonism, Estrogen receptor |
| AOP:382 | Angiotensin II type 1 receptor (AT1R) agonism leading to lung fibrosis | Musculoskeletal system disease; Respiratory system disease | Under Development | 0.17 | KE:1172 | Increased activation, Nuclear factor kappa B (NF-kB) | |
| AOP:419 | Aryl hydrocarbon receptor activation leading to impaired lung function through P53 toxicity pathway | Respiratory system disease | - | 0.25 | KE:1923 | Altered gene expression, P53 dependent apoptosis pathway | |
| AOP:440 | Hypothalamus estrogen receptors activity suppression leading to ovarian cancer via ovarian epithelial cell hyperplasia | Benign neoplasm; Endocrine system disease; Reproductive system disease; Reproductive system disease; Cancer; Endocrine system disease | Under Development | Human, Rat, Mice | 0.11 | KE:1973 | Increased, estrogens |
| AOP:441 | Ionizing radiation-induced DNA damage leads to microcephaly via apoptosis and premature cell differentiation | Congenital nervous system abnormality; Nervous system disease | - | Homo sapiens, Mus musculus musculus, Rattus norvegicus | 0.14 | KE:1974 | Activation of Tumor Protein 53 |
| AOP:443 | DNA damage and mutations leading to Metastatic Breast Cancer | Thoracic disease; Cancer | Under Development | Human and other cells in culture, Human, Mice, Rat, Canine heartworm nematode, Yeast | 0.1 | KE:1172 | Increased activation, Nuclear factor kappa B (NF-kB) |
| AOP:465 | Alcohol dehydrogenase leading to reproductive dysfunction | Unclassified | - | 0.12 | KE:748 | Increased, Estrogen receptor (ER) activity |
| 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:504 | SULT1E1 inhibition leading to uterine adenocarcinoma via increased estrogen availability at target organ level | Unclassified | - | Mammals | 0.33 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:561 | Aromatase induction leading to estrogen receptor alpha activation via increased estradiol | Unclassified | - | Vertebrates | 0.2 | KE:1065 | Activation, estrogen receptor alpha |
| 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:8 | Upregulation of Thyroid Hormone Catabolism via Activation of Hepatic Nuclear Receptors, and Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Nervous system disease | Under Development | Rat | 0.11 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:16 | Acetylcholinesterase inhibition leading to acute mortality | Unclassified | Under Development | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:60 | NR1I2 (Pregnane X Receptor, PXR) activation leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.08 | KE:245 | Activation, PXR/SXR | |
| AOP:167 | Early-life estrogen receptor activity leading to endometrial carcinoma in the mouse. | Reproductive system disease; Cancer | - | Mouse, Homo sapiens | 0.29 | KE:1065 | Activation, estrogen receptor alpha |
| KE:1064 | prepubertal increase, Estrogen receptor (ER) activity | ||||||
| AOP:281 | Acetylcholinesterase Inhibition Leading to Neurodegeneration | Nervous system disease | - | 0.1 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:312 | Acetylcholinesterase Inhibition leading to Acute Mortality via Impaired Coordination & Movement | Unclassified | - | 0.17 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:314 | Binding to estrogen receptor (ER)-α in immune cells leading to exacerbation of systemic lupus erythematosus (SLE) | Immune system disease; Musculoskeletal system disease | Under Development | Homo sapiens | 0.2 | KE:1710 | Binding to estrogen receptor (ER)-α in immune cells |
| AOP:405 | Organo-Phosphate Chemicals induced inhibition of AChE leading to impaired cognitive function | Cognitive disorder | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:445 | Estrogen Receptor Alpha Agonism leads to Impaired Reproduction | Reproductive system disease | - | 0.12 | KE:1065 | Activation, estrogen receptor alpha | |
| AOP:450 | Inhibition of AChE and activation of CYP2E1 leading to sensory axonal peripheral neuropathy and mortality | Nervous system disease | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:493 | ERa inactivation alters AT expansion and functions and leads to insulin resistance and metabolically unhealthy obesity | Acquired metabolic disease | - | Mus musculus, Homo sapiens | 0.1 | KE:2126 | Estrogen receptor alpha inactivation |
| AOP:497 | ERa inactivation alters mitochondrial functions and insulin signalling in skeletal muscle and leads to insulin resistance and metabolic syndrome | Inherited metabolic disorder; Disease of metabolism | - | 0.12 | KE:2126 | Estrogen receptor alpha inactivation | |
| AOP:503 | Activation of uterine estrogen receptor-alfa leading to endometrial adenocarcinoma, via epigenetic modulation | Reproductive system disease; Cancer | Under Review | Human, Mouse | 0.17 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:517 | Pregnane X Receptor (PXR) activation leads to liver steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | Vertebrates | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:536 | Estrogen receptor agonism leading to reduced survival and population growth due to renal failure | Unclassified | - | 0.17 | KE:111 | Agonism, Estrogen receptor | |
| AOP:537 | Estrogen receptor agonism leads to reduced fecundity via increased vitellogenin in the liver | Unclassified | - | 0.2 | KE:111 | Agonism, Estrogen receptor | |
| AOP:545 | Activation, Pregnane-X receptor, NR1l2 leads to increased plasma low-density lipoprotein (LDL) cholesterol via increased cholesterol synthesis | Unclassified | - | Mammals | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:548 | Activation, Pregnane-X receptor, NR1l2 leads to increased plasma low-density lipoprotein (LDL) cholesterol via increased PCSK9 protein expression | Unclassified | - | Mammals | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:559 | Inhibition of acetylcholinesterase (AChE) leading to arrhythmias | Symptom | - | Human and other cells in culture, Rattus norvegicus, Dogs, Sus scrofa, Zebrafish, Insecta sp. BOLD:AAN5199 | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
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.