| 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: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:73 | Xenobiotic Inhibition of Dopamine-beta-Hydroxylase and subsequent reduced fecundity | Unclassified | - | 0.15 | KE:10059 | Decreased LH surge for 24 hours | |
| KE:531 | Decreased, LH Surge | ||||||
| AOP:102 | Cyclooxygenase inhibition leading to reproductive dysfunction via interference with meiotic prophase I /metaphase I transition | Reproductive system disease | - | Goldfish, Human, Rat, Mouse | 0.1 | KE:690 | Reduced, Luteinizing hormone (LH), plasma |
| AOP:103 | Cyclooxygenase inhibition leading to reproductive dysfunction via interference with spindle assembly checkpoint | Reproductive system disease | - | Goldfish, Human, Rat, Mouse | 0.1 | KE:690 | Reduced, Luteinizing hormone (LH), plasma |
| 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:126 | Alpha-noradrenergic antagonism leads to reduced fecundity via delayed ovulation | Unclassified | - | 0.15 | KE:10059 | Decreased LH surge for 24 hours | |
| KE:531 | Decreased, LH Surge | ||||||
| AOP:209 | Perturbation of cholesterol and glutathione homeostasis leading to hepatotoxicity: Integrated multi-OMICS approach for building AOP | Gastrointestinal system disease | - | 0.12 | KE:1289 | Perturbation of cholesterol | |
| AOP:219 | Inhibition of CYP7B activity leads to decreased reproductive success via decreased sexual behavior | Unclassified | - | Japanese quail, Cynops pyrrhogaster | 0.17 | KE:1390 | Sexual behavior, decreased |
| 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: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:496 | Androgen receptor agonism leading to reproduction dysfunction （in zebrafish） | Unclassified | - | Zebrafish | 0.1 | KE:1690 | Decrease, circulating testosterone levels |
| 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 |
| AOP:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.08 | KE:2115 | Altered, cholesterol 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.