| 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: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: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:348 | Inhibition of 11β-Hydroxysteroid Dehydrogenase leading to decreased population trajectory | Unclassified | Under Development | Fish | 0.2 | KE:406 | decreased, Fertility |
| AOP:349 | Inhibition of 11β-hydroxylase leading to decresed population trajectory | Unclassified | Under Development | Fish | 0.12 | KE:406 | decreased, Fertility |
| 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:496 | Androgen receptor agonism leading to reproduction dysfunction (in zebrafish) | Unclassified | - | Zebrafish | 0.1 | KE:1690 | Decrease, circulating testosterone levels |
| AOP:504 | SULT1E1 inhibition leading to uterine adenocarcinoma via increased estrogen availability at target organ level | Unclassified | - | Mammals | 0.33 | KE:2251 | Estradiol availability, increased |
| AOP:561 | Aromatase induction leading to estrogen receptor alpha activation via increased estradiol | Unclassified | - | Vertebrates | 0.4 | KE:2294 | Plasma estradiol, increased |
| KE:2251 | Estradiol availability, increased |
| 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:7 | Aromatase (Cyp19a1) reduction leading to impaired fertility in adult female | Reproductive system disease; Endocrine system disease; Reproductive system disease | Under Review | Rat, Mouse, Human | 0.2 | KE:406 | decreased, Fertility |
| AOP:18 | PPARα activation in utero leading to impaired fertility in males | Reproductive system disease | Under Review | Human, Rat, Mouse | 0.25 | KE:1690 | Decrease, circulating testosterone levels |
| KE:406 | decreased, Fertility | ||||||
| AOP:64 | Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male Fertility | Reproductive system disease | - | Rattus norvegicus | 0.29 | KE:1690 | Decrease, circulating testosterone levels |
| KE:406 | decreased, Fertility | ||||||
| AOP:124 | HMG-CoA reductase inhibition leading to decreased fertility | Reproductive system disease | - | Rattus rattus | 0.33 | KE:1690 | Decrease, circulating testosterone levels |
| KE:330 | Decrease, Fertility | ||||||
| AOP:139 | Alkylation of DNA leading to cancer 1 | Cancer | - | Homo sapiens, Mus musculus | 0.25 | KE:885 | Increase, Cancer |
| AOP:345 | Androgen receptor (AR) antagonism leading to decreased fertility in females | Endocrine system disease; Reproductive system disease; Reproductive system disease | Under Development | Mammals | 0.17 | KE:406 | decreased, Fertility |
| AOP:398 | Decreased ALDH1A (RALDH) activity leading to decreased fertility via disrupted meiotic initiation of fetal oogonia | Reproductive system disease | Under Development | Mouse, Rat, Human | 0.17 | KE:406 | decreased, Fertility |
| 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:492 | Glutathione conjugation leading to reproductive dysfunction via oxidative stress | Reproductive system disease | - | Mammals, Fish | 0.2 | KE:406 | decreased, Fertility |
| 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 |
| 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:520 | Retinoic acid receptor agonism during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | Mouse, Rat, Human | 0.2 | KE:2201 | Agonism, Retinoic acid receptor |
| AOP:523 | Retinoic acid receptor agonism during neurodevelopment leading to microcephaly | Congenital nervous system abnormality; Nervous system disease | - | 0.2 | KE:2201 | Agonism, Retinoic acid receptor | |
| AOP:532 | Retinoic acid receptor agonism during cerebellar development leading to impaired locomotor function | Unclassified | - | 0.2 | KE:2201 | Agonism, Retinoic acid receptor |
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.