RGD Reference Report - Endothelial NOS-derived nitric oxide prevents injury resulting from reoxygenation in the hypoxic lung. - Rat Genome Database

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Endothelial NOS-derived nitric oxide prevents injury resulting from reoxygenation in the hypoxic lung.

Authors: Rus, A  Molina, F  Peinado, MA  Del Moral, ML 
Citation: Rus A, etal., Free Radic Res. 2010 Sep;44(9):1027-35.
RGD ID: 4892012
Pubmed: PMID:20815765   (View Abstract at PubMed)
DOI: DOI:10.3109/10715762.2010.498479   (Journal Full-text)

To date, the role that NO derived from endothelial NO synthase (eNOS) plays in the development of the injuries occurring under hypoxia/reoxygenation (H/R) in the lung remains unknown and thus constitutes the subject of the present work. A follow-up study was conducted in Wistar rats submitted to H/R (hypoxia for 30 min; reoxygenation of 0 h, 48 h and 5 days), with or without prior treatment using the eNOS inhibitor L-NIO (20 mg/kg). Lipid peroxidation, apoptosis, protein nitration and NO production (NOx) were analysed. The results showed that L-NIO administration lowered NOx levels in all the experimental groups. Contrarily, the lipid peroxidation level and the percentage of apoptotic cells rose, implying that eNOS-derived NO may have a protective effect against the injuries occurring during H/R in the lung. These findings could open the possibility of future studies to design new therapies for this type of hypoxia based on NO-pharmacology.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Lung Reperfusion Injury  ISONos3 (Rattus norvegicus)4892012; 4892012 RGD 
Lung Reperfusion Injury  IMP 4892012 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nos3  (nitric oxide synthase 3)

Genes (Mus musculus)
Nos3  (nitric oxide synthase 3, endothelial cell)

Genes (Homo sapiens)
NOS3  (nitric oxide synthase 3)


Additional Information