RGD Reference Report - Excess nitric oxide decreases cytochrome P-450 2J4 content and P-450-dependent arachidonic acid metabolism in lungs of rats with acute pneumonia. - Rat Genome Database

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Excess nitric oxide decreases cytochrome P-450 2J4 content and P-450-dependent arachidonic acid metabolism in lungs of rats with acute pneumonia.

Authors: Yaghi, A  Bend, JR  Webb, CD  Zeldin, DC  Weicker, S  Mehta, S  McCormack, DG 
Citation: Yaghi A, etal., Am J Physiol Lung Cell Mol Physiol. 2004 Jun;286(6):L1260-7. Epub 2004 Feb 6.
RGD ID: 1625385
Pubmed: PMID:14766666   (View Abstract at PubMed)
DOI: DOI:10.1152/ajplung.00273.2003   (Journal Full-text)

Recently, we demonstrated that pulmonary CYP2J4 content, a prominent source of EETs and HETEs formation in rat lungs, is reduced in pneumonia. Therefore, the purpose of this study was to determine the role of iNOS-derived NO in reduced pulmonary CYP2J4 protein content and decreased CYP metabolites in pneumonia. Rats were randomized to control, control plus 1400W (iNOS inhibitor), pneumonia, and pneumonia plus 1400W groups. Pseudomonas organisms were injected into lungs of pneumonia rats. At 40 h after surgery, rats were treated with either saline or 1400W for 4 h before death. Venous plasma samples were obtained for measuring nitrites/nitrates (NOx). There was no significant effect of 1400W on blood pressure measured in control or pneumonia rats, whereas 1400W reduced the elevated plasma NOx levels in pneumonia rats by half. CYP primary metabolites of AA formed at significantly lower rates in pulmonary microsomes from pneumonia rats compared with control rats. Treatment of pneumonia rats with 1400W resulted in a significant increase in the rate of formation of pulmonary EETs and omega-terminal HETEs compared with untreated pneumonia rats. The reduction in CYP2J4 protein content in pneumonia lung microsomes was also partially prevented by 1400W. Therefore, excess NO from iNOS decreases the pulmonary production of EETs and omega-HETEs in acute pneumonia. Inhibition of iNOS restores CYP2J4 protein content and CYP activity in acute pneumonia, indicating an important NO-CYP interaction in pulmonary responses to infection. We speculate CYP2J4 and its AA metabolites are involved in the modulation of pulmonary function in health and disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CYP2J2Humanbacterial pneumonia  ISOCyp2j4 (Rattus norvegicus)protein:decreased expression:lungRGD 
Cyp2j4Ratbacterial pneumonia  IEP protein:decreased expression:lungRGD 
Cyp2j6Mousebacterial pneumonia  ISOCyp2j4 (Rattus norvegicus)protein:decreased expression:lungRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cyp2j4  (cytochrome P450, family 2, subfamily j, polypeptide 4)

Genes (Mus musculus)
Cyp2j6  (cytochrome P450, family 2, subfamily j, polypeptide 6)

Genes (Homo sapiens)
CYP2J2  (cytochrome P450 family 2 subfamily J member 2)


Additional Information