Butylated hydroxytoluene


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:12160896
GO:0001836 Release of cytochrome c from mitochondria Increases phenotype PMID:27588890
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:17879260
GO:0006306 Dna methylation Increases phenotype PMID:9780227
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:17879260
GO:0006751 Glutathione catabolic process Increases phenotype PMID:27387968
GO:0006915 Apoptotic process Increases phenotype PMID:10490238; PMID:16201853
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:33017620
GO:0006979 Response to oxidative stress Increases phenotype PMID:12423650; PMID:17487265
GO:0008219 Cell death Increases phenotype PMID:17568748
GO:0008283 Cell population proliferation Decreases phenotype PMID:7928003
GO:0016042 Lipid catabolic process Increases phenotype PMID:17879260; PMID:27588890; PMID:28774209; PMID:33017620
GO:0016049 Cell growth Decreases phenotype PMID:17568748; PMID:17879260
GO:0030308 Negative regulation of cell growth Increases phenotype PMID:27387968
GO:0030521 Androgen receptor signaling pathway Increases phenotype PMID:26812027
GO:0042391 Regulation of membrane potential Decreases phenotype PMID:28774209
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:28774209
GO:0046466 Membrane lipid catabolic process Affects phenotype PMID:11551671; PMID:16201853; PMID:2366755; PMID:6896723; PMID:7841943
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:27387968
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:34105389
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:28774209; PMID:33812015
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:27387968
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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.