| 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: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: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:431 | Increased tumor necrosis factor (TNF) leading to increased risk of gestational diabetes mellitus (GDM) | Inherited metabolic disorder | - | Human | 0.2 | KE:1952 | Abnormal, Glucose homeostasis |
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.