Title : Oleoyl-lysophosphatidylcholine limits endothelial nitric oxide bioavailability by induction of reactive oxygen species.

Pub. Date : 2014

PMID : 25419657






5 Functional Relationships(s)
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1 This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS). Reactive Oxygen Species nitric oxide synthase 3 Homo sapiens
2 This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS). Reactive Oxygen Species nitric oxide synthase 3 Homo sapiens
3 This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS). Reactive Oxygen Species nitric oxide synthase 3 Homo sapiens
4 This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS). Reactive Oxygen Species nitric oxide synthase 3 Homo sapiens
5 The LPC 18:1-induced ROS formation was attenuated by the superoxide scavenger Tiron, as well as by the pharmacological inhibitors of eNOS, NADPH oxidases, flavin-containing enzymes and superoxide dismutase (SOD). Reactive Oxygen Species nitric oxide synthase 3 Homo sapiens