
| Associated High Confidence AOPs |
|---|
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:16 | Acetylcholinesterase inhibition leading to acute mortality | Unclassified | Under Development | 0.14 | KE:445 | Respiratory distress/arrest |
| AOP:21 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via increased COX-2 | Unclassified | WPHA/WNT Endorsed | 0.2 | KE:317 | Altered, Cardiovascular development/function |
| AOP:27 | Cholestatic Liver Injury induced by Inhibition of the Bile Salt Export Pump (ABCB11) | Gastrointestinal System Disease | Under Development | 0.12 | KE:149 | Increase, Inflammation |
| AOP:41 | Sustained AhR Activation leading to Rodent Liver Tumours | Cancer; Gastrointestinal System Disease | Under Review | 0.2 | KE:853 | Changes/Inhibition, Cellular Homeostasis and Apoptosis |
| AOP:94 | Sodium channel inhibition leading to congenital malformations | Unclassified | - | 0.33 | KE:590 | N/A, hypoxia |
| KE:445 | Respiratory distress/arrest | |||||
| AOP:115 | Epithelial cytotoxicity leading to forestomach tumors (in mouse and rat) | Cancer | - | 0.2 | KE:149 | Increase, Inflammation |
| AOP:150 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via reduced VEGF | Unclassified | WPHA/WNT Endorsed | 0.14 | KE:317 | Altered, Cardiovascular development/function |
| AOP:206 | Peroxisome proliferator-activated receptors γ inactivation leading to lung fibrosis | Musculoskeletal System Disease; Respiratory System Disease | Under Development | 0.17 | KE:149 | Increase, Inflammation |
| AOP:209 | Perturbation of cholesterol and glutathione homeostasis leading to hepatotoxicity: Integrated multi-OMICS approach for building AOP | Gastrointestinal System Disease | - | 0.12 | KE:1287 | Glutathione synthesis |
| AOP:280 | α-diketone-induced bronchiolitis obliterans | Musculoskeletal System Disease; Respiratory System Disease | - | 0.14 | KE:149 | Increase, Inflammation |
| AOP:414 | Aryl hydrocarbon receptor activation leading to lung fibrosis through TGF-β dependent fibrosis toxicity pathway | Musculoskeletal System Disease; Respiratory System Disease | - | 0.2 | KE:1920 | Altered gene expression, TGF-β dependent fibrosis pathway |
| AOP:439 | Activation of the AhR leading to metastatic breast cancer | Thoracic Disease; Cancer | Under Development | 0.11 | KE:149 | Increase, Inflammation |
| AOP:446 | PM-related Adverse outcome pathway frameworks on various systems | Respiratory System Disease | - | 0.1 | KE:149 | Increase, Inflammation |
| KE:1250 | Decrease, Lung function | |||||
| AOP:456 | Aryl hydrocarbon receptor activation leading to early life stage mortality via sox9 repression induced cardiovascular toxicity | Unclassified | Under Review | 0.17 | KE:317 | Altered, Cardiovascular development/function |
| AOP:463 | The AOP framwork on silica nanopariticles induced hepatoxicity | Gastrointestinal System Disease | - | 0.09 | KE:149 | Increase, Inflammation |
| AOP:472 | DNA adduct formation leading to kidney failure | Urinary System Disease | - | 0.11 | KE:149 | Increase, Inflammation |
| AOP:505 | Reactive Oxygen Species (ROS) formation leads to cancer via inflammation pathway | Cancer | - | 0.2 | KE:149 | Increase, Inflammation |
| AOP:544 | Inhibition of neuropathy target esterase leading to delayed neuropathy via increased inflammation | Nervous System Disease | - | 0.17 | KE:149 | Increase, Inflammation |
| AOP:546 | Succinate dehydrogenase inactivation leads to cancer through hypoxic-like mechanisms | Cancer | - | 0.2 | KE:590 | N/A, hypoxia |
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:148 | EGFR Activation Leading to Decreased Lung Function | Respiratory System Disease | Under Development | 0.25 | KE:1250 | Decrease, Lung function |
| AOP:149 | Peptide Oxidation Leading to Hypertension | Cardiovascular System Disease | Under Development | 0.1 | KE:952 | Hypertension |
| AOP:220 | Cyp2E1 Activation Leading to Liver Cancer | Cancer; Gastrointestinal System Disease | WPHA/WNT Endorsed | 0.2 | KE:1395 | Liver Cancer |
| AOP:227 | NSAID induced PTGS1 inactivation to gastric ulcer | Gastrointestinal System Disease | - | 0.14 | KE:1385 | Activated, gastric ulcer formation |
| AOP:228 | NSAID induced PTGS2 inactivation to gastric ulcer | Gastrointestinal System Disease | - | 0.2 | KE:1385 | Activated, gastric ulcer formation |
| AOP:302 | Lung surfactant function inhibition leading to decreased lung function | Respiratory System Disease | Under Development | 0.2 | KE:1250 | Decrease, Lung function |
| AOP:379 | Binding to ACE2 leading to thrombosis and disseminated intravascular coagulation | Cardiovascular System Disease | Under Development | 0.14 | KE:1846 | Thrombosis and Disseminated Intravascular Coagulation |
| AOP:384 | Hyperactivation of ACE/Ang-II/AT1R axis leading to chronic kidney disease | Urinary System Disease | - | 0.17 | KE:1603 | Chronic kidney disease |
| AOP:411 | Oxidative stress Leading to Decreased Lung Function | Respiratory System Disease | - | 0.25 | KE:1250 | Decrease, Lung function |
| AOP:418 | Aryl hydrocarbon receptor activation leading to impaired lung function through AHR-ARNT toxicity pathway | Respiratory System Disease | - | 0.2 | KE:1250 | Decrease, Lung function |
| AOP:419 | Aryl hydrocarbon receptor activation leading to impaired lung function through P53 toxicity pathway | Respiratory System Disease | - | 0.25 | KE:1250 | Decrease, Lung function |
| AOP:424 | Oxidative stress Leading to Decreased Lung Function via CFTR dysfunction | Respiratory System Disease | - | 0.17 | KE:1250 | Decrease, Lung function |
| AOP:425 | Oxidative Stress Leading to Decreased Lung Function via Decreased FOXJ1 | Respiratory System Disease | - | 0.17 | KE:1250 | Decrease, Lung function |
| AOP:573 | Inhibition, cytochrome oxidase leads to Increased, pulmonary edema | Respiratory System Disease | - | 0.33 | KE:2316 | Increased, pulmonary edema |
TICToK is a knowledgebase of chemicals found in tattoo inks, compiled from publicly available regulatory and scientific resources. The chemical classifications presented in this knowledgebase are derived from multiple publicly available resources and are provided solely for informational purposes, and they are neither authoritative nor binding. The chemical-AOP mappings compiled in this knowledgebase serve as plausible hypotheses for research, and further experimental validation is required to definitively establish these potential toxicity mechanisms. The authors bear no responsibility for any errors, omissions, or inconsistencies originating from these external sources. Users are advised to exercise independent judgment when interpreting chemical classifications and any other data provided in this resource. Importantly, our sole goal to build this resource on tattoo ink chemicals is to enable future basic research on this topic, and it does not necessarily reflect the views or objectives of our employers or funders.