Title : High glucose-induced tyrosine nitration in endothelial cells: role of eNOS uncoupling and aldose reductase activation.

Pub. Date : 2003 Jul

PMID : 12824263






4 Functional Relationships(s)
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1 High glucose-induced tyrosine nitration in endothelial cells: role of eNOS uncoupling and aldose reductase activation. Glucose aldo-keto reductase family 1 member B Homo sapiens
2 The effects of glucose were more potent: Inhibiting NOS or aldose reductase (AR), scavenging superoxide or peroxynitrite, or supplementing the NOS substrate L-arginine or cofactor tetrahydrobiopterin blocked the formation of reactive oxygen species and prevented protein tyrosine nitration. Glucose aldo-keto reductase family 1 member B Homo sapiens
3 The effects of glucose were more potent: Inhibiting NOS or aldose reductase (AR), scavenging superoxide or peroxynitrite, or supplementing the NOS substrate L-arginine or cofactor tetrahydrobiopterin blocked the formation of reactive oxygen species and prevented protein tyrosine nitration. Glucose aldo-keto reductase family 1 member B Homo sapiens
4 CONCLUSIONS: Increases in glucose levels and osmotic stress similar to those in diabetic patients increase the formation of nitrotyrosine in retinal endothelial cells because of their actions increasing NOS activity and causing superoxide formation due to eNOS uncoupling and AR activation. Glucose aldo-keto reductase family 1 member B Homo sapiens