Sodium nitrite


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001825 Blastocyst formation Decreases phenotype PMID:31476334
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:28266762; PMID:28266762; PMID:33030083; PMID:33030083
GO:0006749 Glutathione metabolic process Increases phenotype PMID:26231821
GO:0006954 Inflammatory response Increases phenotype PMID:33030083
GO:0006979 Response to oxidative stress Increases phenotype PMID:21130833
GO:0007009 Plasma membrane organization Decreases phenotype PMID:26231821
GO:0007058 Spindle assembly involved in female meiosis ii Affects phenotype PMID:31476334
GO:0010729 Positive regulation of hydrogen peroxide biosynthetic process Increases phenotype PMID:26231821
GO:0010867 Positive regulation of triglyceride biosynthetic process Increases phenotype PMID:25183945
GO:0018158 Protein oxidation Increases phenotype PMID:26231821
GO:0018212 Peptidyl-tyrosine modification Affects phenotype PMID:25211009
GO:0020027 Hemoglobin metabolic process Increases phenotype PMID:26231821
GO:0030199 Collagen fibril organization Increases phenotype PMID:33030083
GO:0034440 Lipid oxidation Increases phenotype PMID:26231821
GO:0035803 Egg coat formation Affects phenotype PMID:31476334
GO:0040015 Negative regulation of multicellular organism growth Increases phenotype PMID:31476334
GO:0040016 Embryonic cleavage Decreases phenotype PMID:31476334
GO:0040038 Polar body extrusion after meiotic divisions Decreases phenotype PMID:31476334
GO:0042311 Vasodilation Decreases phenotype PMID:25841777
GO:0042541 Hemoglobin biosynthetic process Decreases phenotype PMID:28266762; PMID:28833918
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:28000380; PMID:31476334
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32671443
GO:0044648 Histone h3-k4 dimethylation Increases phenotype PMID:31476334
GO:0045542 Positive regulation of cholesterol biosynthetic process Increases phenotype PMID:25183945
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:31476334
GO:0046622 Positive regulation of organ growth Increases phenotype PMID:31476334
GO:0046889 Positive regulation of lipid biosynthetic process Increases phenotype PMID:25183945
GO:0048312 Intracellular distribution of mitochondria Affects phenotype PMID:31476334
GO:0048872 Homeostasis of number of cells Decreases phenotype PMID:31476334
GO:0050996 Positive regulation of lipid catabolic process Increases phenotype PMID:25183945
GO:0051260 Protein homooligomerization Decreases phenotype PMID:25211009
GO:0051897 Positive regulation of protein kinase b signaling Increases phenotype PMID:28000380
GO:0051988 Regulation of attachment of spindle microtubules to kinetochore Decreases phenotype PMID:31476334
GO:0060467 Negative regulation of fertilization Increases phenotype PMID:31476334
GO:0070994 Detection of oxidative stress Increases phenotype PMID:33030083
GO:0097009 Energy homeostasis Decreases phenotype PMID:31476334
GO:1900194 Negative regulation of oocyte maturation Increases phenotype PMID:31476334
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:25183945
GO:1901671 Positive regulation of superoxide dismutase activity Decreases phenotype PMID:26231821
GO:1903283 Negative regulation of glutathione peroxidase activity Increases phenotype PMID:25183945
GO:1903284 Positive regulation of glutathione peroxidase activity Decreases phenotype PMID:26231821
GO:1903301 Positive regulation of hexokinase activity Decreases phenotype PMID:26231821
GO:1903408 Positive regulation of p-type sodium:potassium-exchanging transporter activity Decreases phenotype PMID:26231821
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:31476334
GO:1903787 Negative regulation of glutathione biosynthetic process Increases phenotype PMID:25183945
GO:1905376 Negative regulation of cytochrome-c oxidase activity Increases phenotype PMID:21751223
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.