7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001836 Release of cytochrome c from mitochondria Increases phenotype PMID:24837741
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:36450496; PMID:39826883
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:36450496
GO:0006171 Camp biosynthetic process Affects phenotype PMID:32115946
GO:0006304 Dna modification Increases phenotype PMID:26238291
GO:0006749 Glutathione metabolic process Affects phenotype PMID:36450496; PMID:39826883
GO:0006879 Cellular iron ion homeostasis Affects phenotype PMID:39826883
GO:0006915 Apoptotic process Increases phenotype PMID:28529061
GO:0006954 Inflammatory response Increases phenotype PMID:37436145
GO:0006974 Cellular response to dna damage stimulus Affects phenotype PMID:24269554; PMID:28593498; PMID:34454013
GO:0007005 Mitochondrion organization Decreases phenotype PMID:36450496; PMID:39826883
GO:0008219 Cell death Increases phenotype PMID:28593498
GO:0008283 Cell population proliferation Increases phenotype PMID:34454013; PMID:39287666
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:30453383; PMID:34196753; PMID:35038060
GO:0010587 Mirna catabolic process Increases phenotype PMID:35038060
GO:0010917 Negative regulation of mitochondrial membrane potential Increases phenotype PMID:37579952
GO:0010918 Positive regulation of mitochondrial membrane potential Decreases phenotype PMID:35940284
GO:0010942 Positive regulation of cell death Increases phenotype PMID:28077981
GO:0014902 Myotube differentiation Decreases phenotype PMID:24431215
GO:0016477 Cell migration Increases phenotype PMID:39287666
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:36450496
GO:0032205 Negative regulation of telomere maintenance Increases phenotype PMID:37579952
GO:0032310 Prostaglandin secretion Affects phenotype PMID:32115946
GO:0032981 Mitochondrial respiratory chain complex i assembly Decreases phenotype PMID:37579952
GO:0034440 Lipid oxidation Increases phenotype PMID:39826883
GO:0042770 Signal transduction in response to dna damage Increases phenotype PMID:30453383
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:37579952
GO:0044237 Cellular metabolic process Decreases phenotype PMID:24837741; PMID:34454013; PMID:36450496; PMID:39826883
GO:0044319 Wound healing, spreading of cells Decreases phenotype PMID:28529061
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:28529061; PMID:35038060
GO:0051402 Neuron apoptotic process Increases phenotype PMID:32115946
GO:0051490 Negative regulation of filopodium assembly Increases phenotype PMID:30011042
GO:0055072 Iron ion homeostasis Affects phenotype PMID:36450496
GO:0060326 Cell chemotaxis Increases phenotype PMID:34610339; PMID:39287666
GO:0070265 Necrotic cell death Affects phenotype PMID:24837741
GO:0070987 Error-free translesion synthesis Increases phenotype PMID:28077981
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:36450496
GO:0090298 Negative regulation of mitochondrial dna replication Increases phenotype PMID:37579952
GO:0097707 Ferroptosis Increases phenotype PMID:36450496
GO:0140639 Positive regulation of pyroptosis Increases phenotype PMID:35297523
GO:0140742 Lncrna transcription Increases phenotype PMID:35038060
GO:1901164 Negative regulation of trophoblast cell migration Increases phenotype PMID:30011042
GO:1901987 Regulation of cell cycle phase transition Affects phenotype PMID:37579952
GO:1902808 Positive regulation of cell cycle g1/s phase transition Increases phenotype PMID:37579952
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:28529061
GO:2000774 Positive regulation of cellular senescence Increases phenotype PMID:37579952
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.