Methanol

Methanol



Associated High Confidence AOPs
For more information or term definitions, please refer to HELP page.

Navigate to: Level 1Level 2Level 3Level 5

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 Coverage Score KE Identifier KE Name
AOP:48Binding of agonists to ionotropic glutamate receptors in adult brain causes excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment.Developmental Disorder Of Mental HealthWPHA/WNT Endorsed0.11KE:352
N/A, Neurodegeneration
AOP:975-hydroxytryptamine transporter (5-HTT; SERT) inhibition leading to population declineUnclassified-0.1KE:626
Increased, serotonin (5-HT)
AOP:985-hydroxytryptamine transporter (5-HTT; SERT) inhibition leading to decreased shelter seeking and increased predationUnclassified-0.2KE:626
Increased, serotonin (5-HT)
AOP:1955-hydroxytryptamine transporter (5-HTT) inhibition leading to population increaseUnclassified-0.12KE:626
Increased, serotonin (5-HT)
AOP:2035-hydroxytryptamine transporter inhibition leading to decreased reproductive success and population declineReproductive System Disease-0.12KE:626
Increased, serotonin (5-HT)
AOP:2045-hydroxytryptamine transporter inhibition leading to increased reproductive success and population increaseUnclassified-0.12KE:626
Increased, serotonin (5-HT)
AOP:321Reduced environmental pH leading to thinner shells in Mytilus edulisUnclassified-0.09KE:10042
Abnormal development
AOP:372Androgen receptor antagonism leading to testicular cancerEndocrine System Disease; Reproductive System Disease; Cancer-0.2KE:1616
Malformation, cryptorchidism - maldescended testis
AOP:374Binding of Sars-CoV-2 spike protein to ACE 2 receptors expressed on brain cells (neuronal and non-neuronal) leads to neuroinflammation resulting in encephalitisNervous System DiseaseUnder Development0.25KE:352
N/A, Neurodegeneration
AOP:450Inhibition of AChE and activation of CYP2E1 leading to sensory axonal peripheral neuropathy and mortalityNervous System Disease-0.14KE:352
N/A, Neurodegeneration
AOP:500Activation of MEK-ERK1/2 leads to deficits in learning and cognition via ROS and apoptosisDevelopmental Disorder Of Mental Health-0.14KE:352
N/A, Neurodegeneration
AOP:520Retinoic acid receptor agonism during neurodevelopment leading to impaired learning and memoryDevelopmental Disorder Of Mental Health-0.2KE:2204
Altered brain morphology
AOP:550Increased LMNA gene mutation leading to heart failureCardiovascular System Disease-0.2KE:2066
Altered Signaling Pathways
AOP:568Inhibition, 5-hydroxytryptamine transporter (5-HTT; SERT) leads to Inhibition, FeedingUnclassified-0.25KE:1320
Increased, extracellular serotonin
AOP:569Decreased DNA methylation of FAM50B/PTCHD3 leading to IQ loss of children via PI3K-Akt pathwayDevelopmental Disorder Of Mental Health-0.17KE:2195
Increase, CNS Neural cell death

Associated AOPs with Level of Relevance 2
AOPs with at least 1 AO associated with chemical, and no associated MIE
AOP Identifier AOP Title AO Classification OECD Status Coverage Score KE Identifier KE Name
AOP:12Chronic binding of antagonist to N-methyl-D-aspartate receptors (NMDARs) during brain development leads to neurodegeneration with impairment in learning and memory in agingNervous System Disease; Developmental Disorder Of Mental HealthWPHA/WNT Endorsed0.12KE:352
N/A, Neurodegeneration
AOP:260CYP2E1 activation and formation of protein adducts leading to neurodegenerationNervous System Disease-0.14KE:1514
Neurodegeneration
AOP:269Elevated ATP demand for detoxification and repair mechanisms leading to impaired growth and developmentUnclassified-0.17KE:10013
Impaired growth and development
AOP:270Elevated ATP demand for detoxification and repair mechanisms leading to impaired locomotor activityUnclassified-0.12KE:10016
Impaired locomotor activity
AOP:281Acetylcholinesterase Inhibition Leading to NeurodegenerationNervous System Disease-0.1KE:352
N/A, Neurodegeneration
AOP:288Inhibition of 17α-hydrolase/C 10,20-lyase (Cyp17A1) activity leads to birth reproductive defects (cryptorchidism) in male (mammals)Endocrine System Disease-0.12KE:1616
Malformation, cryptorchidism - maldescended testis
AOP:498Increased LCN2/iron complex leading to neurological disordersNervous System Disease-0.25KE:2150
Neurological disorder
AOP:501Excessive iron accumulation leading to neurological disordersNervous System Disease-0.25KE:2150
Neurological disorder
AOP:532Retinoic acid receptor agonism during cerebellar development leading to impaired locomotor functionUnclassified-0.2KE:2231
Locomotor function. Impaired

No associated AOPs with Level of Relevance 3

No associated AOPs with Level of Relevance 5
Glossary of Terms
AOP
Adverse Outcome Pathway
MIE
Molecular Initiating Event
KE
Key Event
AO
Adverse Outcome
Coverage score
The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints
Level of relevance
Qualitative rank based on the kind of associated KEs within the corresponding AOP
AO classification
The disease category corresponding to the AO in the AOP obtained from Disease Ontology
?
DISCLAIMER

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.