RGD Reference Report - Nitric oxide (no), citrulline - no cycle enzymes, glutamine synthetase and oxidative stress in anoxia (hypobaric hypoxia) and reperfusion in rat brain. - Rat Genome Database

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Nitric oxide (no), citrulline - no cycle enzymes, glutamine synthetase and oxidative stress in anoxia (hypobaric hypoxia) and reperfusion in rat brain.

Authors: Swamy, M  Salleh, MJ  Sirajudeen, KN  Yusof, WR  Chandran, G 
Citation: Swamy M, etal., Int J Med Sci. 2010 May 31;7(3):147-54.
RGD ID: 4110824
Pubmed: PMID:20567615   (View Abstract at PubMed)
PMCID: PMC2880843   (View Article at PubMed Central)

Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders due to hypoxia/ anoxia in brain due to increased release of glutamate and activation of N-methyl-D-aspartate receptors. Reactive oxygen species have been implicated in pathophysiology of many neurological disorders and in brain function. To understand their role in anoxia (hypobaric hypoxia) and reperfusion (reoxygenation), the nitric oxide synthase, argininosuccinate synthetase, argininosuccinate lyase, glutamine synthetase and arginase activities along with the concentration of nitrate /nitrite, thiobarbituric acid reactive substances and total antioxidant status were estimated in cerebral cortex, cerebellum and brain stem of rats subjected to anoxia and reperfusion. The results of this study clearly demonstrated the increased production of nitric oxide by increased activity of nitric oxide synthase. The increased activities of argininosuccinate synthetase and argininosuccinate lyase suggest the increased and effective recycling of citrulline to arginine in anoxia, making nitric oxide production more effective and contributing to its toxic effects. The decreased activity of glutamine synthetase may favor the prolonged availability of glutamic acid causing excitotoxicity leading to neuronal damage in anoxia. The increased formation of thiobarbituric acid reactive substances and decreased total antioxidant status indicate the presence of oxidative stress in anoxia and reperfusion. The increased arginase and sustained decrease of GS activity in reperfusion group likely to be protective.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hypoxia  ISOAsl (Rattus norvegicus)4110824; 4110824protein:increased activity:brain (rat)RGD 
Hypoxia  ISOAss1 (Rattus norvegicus)4110824; 4110824protein:increased activity:brain (rat)RGD 
Hypoxia  IEP 4110824; 4110824protein:increased activity:brain (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Asl  (argininosuccinate lyase)
Ass1  (argininosuccinate synthase 1)

Genes (Mus musculus)
Asl  (argininosuccinate lyase)
Ass1  (argininosuccinate synthetase 1)

Genes (Homo sapiens)
ASL  (argininosuccinate lyase)
ASS1  (argininosuccinate synthase 1)


Additional Information