Carbon black
| Associated High Confidence AOPs |
|---|
Associated AOPs with Level of Relevance 1
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:27 | Cholestatic Liver Injury induced by Inhibition of the Bile Salt Export Pump (ABCB11) | Gastrointestinal System Disease | Under Development | 0.12 | KE:1115 | Increase, Reactive oxygen species |
| AOP:39 | Covalent Binding, Protein, leading to Increase, Allergic Respiratory Hypersensitivity Response | Respiratory System Disease | Under Development | 0.2 | KE:1496 | Increased, secretion of proinflammatory mediators |
| AOP:136 | Intracellular Acidification Induced Olfactory Epithelial Injury Leading to Site of Contact Nasal Tumors | Benign Neoplasm; Respiratory System Disease | Under Review | 0.14 | KE:870 | Increase, Cell Proliferation |
| AOP:207 | NADPH oxidase and P38 MAPK activation leading to reproductive failure in Caenorhabditis elegans | Reproductive System Disease | - | 0.12 | KE:1115 | Increase, Reactive oxygen species |
| AOP:213 | Inhibition of fatty acid beta oxidation leading to nonalcoholic steatohepatitis (NASH) | Gastrointestinal System Disease; Inherited Metabolic Disorder | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:272 | Deposition of energy leading to lung cancer | Cancer | WPHA/WNT Endorsed | 0.14 | KE:870 | Increase, Cell Proliferation |
| AOP:299 | Deposition of energy leading to population decline via DNA oxidation and follicular atresia | Unclassified | - | 0.14 | KE:1115 | Increase, Reactive oxygen species |
| AOP:311 | Deposition of energy leading to population decline via DNA oxidation and oocyte apoptosis | Unclassified | - | 0.14 | KE:1115 | Increase, Reactive oxygen species |
| AOP:320 | Binding of SARS-CoV-2 to ACE2 receptor leading to acute respiratory distress associated mortality | Unclassified | Under Development | 0.11 | KE:1496 | Increased, secretion of proinflammatory mediators |
| AOP:382 | Angiotensin II type 1 receptor (AT1R) agonism leading to lung fibrosis | Musculoskeletal System Disease; Respiratory System Disease | Under Development | 0.33 | KE:1115 | Increase, Reactive oxygen species |
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| AOP:383 | Inhibition of Angiotensin-converting enzyme 2 leading to liver fibrosis | Gastrointestinal System Disease | Under Development | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:384 | Hyperactivation of ACE/Ang-II/AT1R axis leading to chronic kidney disease | Urinary System Disease | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:386 | Deposition of ionizing energy leading to population decline via inhibition of photosynthesis | Reproductive System Disease | - | 0.12 | KE:1115 | Increase, Reactive oxygen species |
| AOP:387 | Deposition of ionising energy leading to population decline via mitochondrial dysfunction | Reproductive System Disease | - | 0.12 | KE:1115 | Increase, Reactive oxygen species |
| AOP:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | 0.4 | KE:1497 | Increased, recruitment of inflammatory cells |
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| AOP:409 | Frustrated phagocytosis leads to malignant mesothelioma | Cancer | - | 0.62 | KE:1669 | Increased, DNA damage and mutation |
| KE:870 | Increase, Cell Proliferation | |||||
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| KE:1115 | Increase, Reactive oxygen species | |||||
| KE:1497 | Increased, recruitment of inflammatory cells | |||||
| AOP:413 | Oxidation and antagonism of reduced glutathione leading to mortality via acute renal failure | Unclassified | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:418 | Aryl hydrocarbon receptor activation leading to impaired lung function through AHR-ARNT toxicity pathway | Respiratory System Disease | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:432 | Deposition of Energy by Ionizing Radiation leading to Acute Myeloid Leukemia | Hematopoietic System Disease; Cancer | - | 0.09 | KE:870 | Increase, Cell Proliferation |
| AOP:468 | Binding of SARS-CoV-2 to ACE2 leads to hyperinflammation (via cell death) | Unclassified | - | 0.25 | KE:1497 | Increased, recruitment of inflammatory cells |
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| AOP:478 | Deposition of energy leading to occurrence of cataracts | Nervous System Disease; Monogenic Disease | Under Review | 0.1 | KE:870 | Increase, Cell Proliferation |
| AOP:492 | Glutathione conjugation leading to reproductive dysfunction via oxidative stress | Reproductive System Disease | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:493 | ERa inactivation alters AT expansion and functions and leads to insulin resistance and metabolically unhealthy obesity | Acquired Metabolic Disease | - | 0.1 | KE:1497 | Increased, recruitment of inflammatory cells |
| AOP:497 | ERa inactivation alters mitochondrial functions and insulin signalling in skeletal muscle and leads to insulin resistance and metabolic syndrome | Inherited Metabolic Disorder; Disease Of Metabolism | - | 0.12 | KE:1115 | Increase, Reactive oxygen species |
| AOP:500 | Activation of MEK-ERK1/2 leads to deficits in learning and cognition via ROS and apoptosis | Developmental Disorder Of Mental Health | - | 0.14 | KE:1115 | Increase, Reactive oxygen species |
| AOP:521 | Essential element imbalance leads to reproductive failure via oxidative stress | Unclassified | - | 0.14 | KE:1115 | Increase, Reactive oxygen species |
| AOP:534 | Succinate dehydrogenase (SDH) inhibition leads to cancer through oxidative stress | Cancer | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:569 | Decreased DNA methylation of FAM50B/PTCHD3 leading to IQ loss of children via PI3K-Akt pathway | Developmental Disorder Of Mental Health | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
Associated AOPs with Level of Relevance 2
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:303 | Frustrated phagocytosis-induced lung cancer | Cancer | Under Development | 0.71 | KE:1669 | Increased, DNA damage and mutation |
| KE:870 | Increase, Cell Proliferation | |||||
| KE:1670 | Lung cancer | |||||
| KE:1115 | Increase, Reactive oxygen species | |||||
| KE:1497 | Increased, recruitment of inflammatory cells | |||||
| AOP:416 | Aryl hydrocarbon receptor activation leading to lung cancer through IL-6 toxicity pathway | Cancer | - | 0.5 | KE:1669 | Increased, DNA damage and mutation |
| KE:1115 | Increase, Reactive oxygen species | |||||
| KE:1670 | Lung cancer | |||||
| AOP:417 | Aryl hydrocarbon receptor activation leading to lung cancer through AHR-ARNT toxicity pathway | Cancer | - | 0.4 | KE:1669 | Increased, DNA damage and mutation |
| KE:1670 | Lung cancer | |||||
| AOP:420 | Aryl hydrocarbon receptor activation leading to lung cancer through sustained NRF2 toxicity pathway | Cancer | - | 0.5 | KE:870 | Increase, Cell Proliferation |
| KE:1670 | Lung cancer |
Associated AOPs with Level of Relevance 3
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:115 | Epithelial cytotoxicity leading to forestomach tumors (in mouse and rat) | Cancer | - | 0.2 | KE:780 | Increase, Cytotoxicity (epithelial cells) |
| AOP:173 | Substance interaction with the pulmonary resident cell membrane components leading to pulmonary fibrosis | Musculoskeletal System Disease; Respiratory System Disease | WPHA/WNT Endorsed | 0.38 | KE:1495 | Substance interaction with the lung resident cell membrane components |
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| KE:1497 | Increased, recruitment of inflammatory cells | |||||
| AOP:237 | Substance interaction with lung resident cell membrane components leading to atherosclerosis | Cardiovascular System Disease | Under Development | 0.4 | KE:1495 | Substance interaction with the lung resident cell membrane components |
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| AOP:282 | Adverse outcome pathway on photochemical toxicity initiated by light exposure | Unclassified | Under Review | 0.25 | KE:1115 | Increase, Reactive oxygen species |
| AOP:298 | Increase in reactive oxygen species (ROS) leading to human treatment-resistant gastric cancer via chronic ROS | Cancer; Gastrointestinal System Disease | Under Review | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:324 | Excessive reactive oxygen species leading to growth inhibition via oxidative DNA damage and cell death | Unclassified | - | 0.25 | KE:1115 | Increase, Reactive oxygen species |
| AOP:325 | Excessive reactive oxygen species leading to growth inhibition via lipid peroxidation and cell death | Unclassified | - | 0.25 | KE:1115 | Increase, Reactive oxygen species |
| AOP:326 | Excessive reactive oxygen species leading to growth inhibition via protein oxidation and cell death | Unclassified | - | 0.25 | KE:1115 | Increase, Reactive oxygen species |
| AOP:327 | Excessive reactive oxygen species production leading to mortality (1) | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:328 | Excessive reactive oxygen species production leading to mortality (2) | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:329 | Excessive reactive oxygen species production leading to mortality (3) | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:330 | Excessive reactive oxygen species production leading to mortality (4) | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:331 | Excessive reactive oxygen species leading to growth inhibition via oxidative DNA damage and reduced cell proliferation | Unclassified | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:332 | Excessive reactive oxygen species leading to growth inhibition via lipid peroxidation and reduced cell proliferation | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:333 | Excessive reactive oxygen species leading to growth inhibition via uncoupling of oxidative phosphorylation | Unclassified | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:423 | Toxicological mechanisms of hepatocyte apoptosis through the PARP1 dependent cell death pathway | Unclassified | - | 0.17 | KE:1115 | Increase, Reactive oxygen species |
| AOP:438 | reactive oxygen species generation leading to increased cardiovascular morbidity and mortality | Cardiovascular System Disease | - | 0.08 | KE:1115 | Increase, Reactive oxygen species |
| AOP:443 | DNA damage and mutations leading to Metastatic Breast Cancer | Thoracic Disease; Cancer | Under Development | 0.1 | KE:1669 | Increased, DNA damage and mutation |
| AOP:446 | PM-related Adverse outcome pathway frameworks on various systems | Respiratory System Disease | - | 0.15 | KE:1115 | Increase, Reactive oxygen species |
| KE:1497 | Increased, recruitment of inflammatory cells | |||||
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| AOP:448 | ROS, inflammation, and activation of nAChR lead to increased incidence of cardiovascular morbidity and mortality | Cardiovascular System Disease | - | 0.06 | KE:1115 | Increase, Reactive oxygen species |
| 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:1115 | Increase, Reactive oxygen species |
| AOP:463 | The AOP framwork on silica nanopariticles induced hepatoxicity | Gastrointestinal System Disease | - | 0.09 | KE:1115 | Increase, Reactive oxygen species |
| AOP:469 | Reactive oxygen speicies overproduction leading to increased digestive morbidity and mortality in generation population | Gastrointestinal System Disease | - | 0.08 | KE:1115 | Increase, Reactive oxygen species |
| AOP:472 | DNA adduct formation leading to kidney failure | Urinary System Disease | - | 0.11 | KE:1115 | Increase, Reactive oxygen species |
| AOP:488 | Increased reactive oxygen species production leading to decreased cognitive function | Cognitive Disorder | - | 0.14 | KE:1115 | Increase, Reactive oxygen species |
| AOP:505 | Reactive Oxygen Species (ROS) formation leads to cancer via inflammation pathway | Cancer | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:511 | The AOP framework on ROS-mediated oxidative stress induced vascular disrupting effects | Cardiovascular System Disease | - | 0.06 | KE:1115 | Increase, Reactive oxygen species |
| AOP:513 | Reactive Oxygen (ROS) formation leads to cancer via Peroxisome proliferation-activated receptor (PPAR) pathway | Cancer | - | 0.2 | KE:1115 | Increase, Reactive oxygen species |
| AOP:540 | Oxidative Stress in the Fish Ovary Leads to Reproductive Impairment via Reduced Vitellogenin Production | Unclassified | - | 0.11 | KE:1115 | Increase, Reactive oxygen species |
| AOP:541 | Excessive ROS generation leading to increased incidence of vascular calcification by VSMC phenotype switching | Cardiovascular System Disease | - | 0.08 | KE:1115 | Increase, Reactive oxygen species |
Associated AOPs with Level of Relevance 5
| AOP Identifier | AOP Title | AO Classification | OECD Status | Coverage Score | KE Identifier | KE Name |
|---|---|---|---|---|---|---|
| AOP:451 | Interaction with lung resident cell membrane components leads to lung cancer | Cancer | - | 1.0 | KE:1495 | Substance interaction with the lung resident cell membrane components |
| KE:1669 | Increased, DNA damage and mutation | |||||
| KE:870 | Increase, Cell Proliferation | |||||
| KE:2006 | Secondary genotoxicity | |||||
| KE:1496 | Increased, secretion of proinflammatory mediators | |||||
| KE:1670 | Lung cancer | |||||
| KE:1115 | Increase, Reactive oxygen species | |||||
| KE:780 | Increase, Cytotoxicity (epithelial cells) | |||||
| KE:1497 | Increased, recruitment of inflammatory cells |
DISCLAIMER
TICToK is a database of tattoo ink chemicals compiled from different regulatory resources. The authors are not liable for any inaccuracies or omissions of any chemicals 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.