Palladium


Associated AOPs with Level of Relevance - 1 AOPs with at least 1 KE associated with chemical, where the KE(s) are neither MIE nor AO

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:7Aromatase (Cyp19a1) reduction leading to impaired fertility in adult femaleReproductive system disease; Endocrine system disease; Reproductive system diseaseUnder ReviewRat, Mouse, Human0.4KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:18PPARα activation in utero leading to impaired fertility in malesReproductive system diseaseUnder ReviewHuman, Rat, Mouse0.12KE:1690Decrease, circulating testosterone levels
AOP:23Androgen receptor agonism leading to reproductive dysfunction (in repeat-spawning fish)UnclassifiedWPHA/WNT EndorsedPimephales promelas0.2KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:25Aromatase inhibition leading to reproductive dysfunctionUnclassifiedWPHA/WNT EndorsedFathead minnow, Medaka, Zebrafish0.25KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:64Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male FertilityReproductive system disease-Rattus norvegicus0.14KE:1690Decrease, circulating testosterone levels
AOP:73Xenobiotic Inhibition of Dopamine-beta-Hydroxylase and subsequent reduced fecundityUnclassified-0.15KE:10059Decreased LH surge for 24 hours
KE:531Decreased, LH Surge
AOP:102Cyclooxygenase inhibition leading to reproductive dysfunction via interference with meiotic prophase I /metaphase I transitionReproductive system disease-Goldfish, Human, Rat, Mouse0.1KE:690Reduced, Luteinizing hormone (LH), plasma
AOP:103Cyclooxygenase inhibition leading to reproductive dysfunction via interference with spindle assembly checkpointReproductive system disease-Goldfish, Human, Rat, Mouse0.1KE:690Reduced, Luteinizing hormone (LH), plasma
AOP:111Decrease in androgen receptor activity leading to Leydig cell tumors (in rat)Cancer; Reproductive system disease-Rattus norvegicus0.2KE:754Increased, Luteinizing hormone (LH)
AOP:120Inhibition of 5α-reductase leading to Leydig cell tumors (in rat)Cancer; Reproductive system disease-Rattus norvegicus, Mus musculus0.4KE:791Increased, Leutinizing hormone (LH)
KE:1690Decrease, circulating testosterone levels
AOP:122Prolyl hydroxylase inhibition leading to reproductive dysfunction via increased HIF1 heterodimer formationUnclassified-Pimephales promelas0.2KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:123Unknown MIE leading to reproductive dysfunction via increased HIF-1alpha transcriptionUnclassified-Pimephales promelas0.18KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:124HMG-CoA reductase inhibition leading to decreased fertilityReproductive system disease-Rattus rattus0.17KE:1690Decrease, circulating testosterone levels
AOP:126Alpha-noradrenergic antagonism leads to reduced fecundity via delayed ovulationUnclassified-0.15KE:10059Decreased LH surge for 24 hours
KE:531Decreased, LH Surge
AOP:271Inhibition of thyroid peroxidase leading to impaired fertility in fishUnclassifiedUnder DevelopmentFish0.2KE:219Reduction, Plasma 17beta-estradiol concentrations
AOP:288Inhibition of 17α-hydrolase/C 10,20-lyase (Cyp17A1) activity leads to birth reproductive defects (cryptorchidism) in male (mammals)Endocrine system disease-Human, Rat0.12KE:1690Decrease, circulating testosterone levels
AOP:289Inhibition of 5α-reductase leading to impaired fecundity in female fishUnclassifiedUnder DevelopmentFish0.17KE:219Reduction, Plasma 17beta-estradiol concentrations
AOP:310Embryonic Activation of the AHR leading to Reproductive failure, via epigenetic down-regulation of GnRHRUnclassified-Zebrafish0.17KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:346Aromatase inhibition leads to male-biased sex ratio via impacts on gonad differentiationUnclassifiedWPHA/WNT EndorsedZebrafish, Oreochromis niloticus, Chinook salmon, Fathead minnow, European sea bass0.2KE:1789Reduction, 17beta-estradiol synthesis by the undifferentiated gonad
AOP:496Androgen receptor agonism leading to reproduction dysfunction （in zebrafish）Unclassified-Zebrafish0.2KE:219Reduction, Plasma 17beta-estradiol concentrations
KE:1690Decrease, circulating testosterone levels
AOP:540Oxidative Stress in the Fish Ovary Leads to Reproductive Impairment via Reduced Vitellogenin ProductionUnclassified-0.11KE:3Reduction, 17beta-estradiol synthesis by ovarian granulosa cells
AOP:549Aromatase inhibition leads to reproductive toxicity (including growth and developmental toxicity) in adult female zebrafishUnclassified-0.12KE:219Reduction, Plasma 17beta-estradiol concentrations

No associated AOPs with Level of Relevance 2

No associated AOPs with Level of Relevance 3

No associated AOPs with Level of Relevance 5
DISCLAIMER

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.