Show simple item record

dc.contributor.author Yao, JK
dc.contributor.author Dougherty, GG
dc.contributor.author Reddy, RD
dc.contributor.author Keshavan, MS
dc.contributor.author Montrose, DM
dc.contributor.author Matson, WR
dc.contributor.author McEvoy, J
dc.contributor.author Kaddurah-Daouk, R
dc.coverage.spatial United States
dc.date.accessioned 2011-06-21T17:31:29Z
dc.date.issued 2010-03-03
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20209081
dc.identifier.citation PLoS One, 2010, 5 (3), pp. e9508 - ?
dc.identifier.uri http://hdl.handle.net/10161/4529
dc.description.abstract BACKGROUND: Purine catabolism may be an unappreciated, but important component of the homeostatic response of mitochondria to oxidant stress. Accumulating evidence suggests a pivotal role of oxidative stress in schizophrenia pathology. METHODOLOGY/PRINCIPAL FINDINGS: Using high-pressure liquid chromatography coupled with a coulometric multi-electrode array system, we compared 6 purine metabolites simultaneously in plasma between first-episode neuroleptic-naïve patients with schizophrenia (FENNS, n = 25) and healthy controls (HC, n = 30), as well as between FENNS at baseline (BL) and 4 weeks (4w) after antipsychotic treatment. Significantly higher levels of xanthosine (Xant) and lower levels of guanine (G) were seen in both patient groups compared to HC subjects. Moreover, the ratios of G/guanosine (Gr), uric acid (UA)/Gr, and UA/Xant were significantly lower, whereas the ratio of Xant/G was significantly higher in FENNS-BL than in HC. Such changes remained in FENNS-4w with exception that the ratio of UA/Gr was normalized. All 3 groups had significant correlations between G and UA, and Xan and hypoxanthine (Hx). By contrast, correlations of UA with each of Xan and Hx, and the correlation of Xan with Gr were all quite significant for the HC but not for the FENNS. Finally, correlations of Gr with each of UA and G were significant for both HC and FENNS-BL but not for the FENNS-4w. CONCLUSIONS/SIGNIFICANCE: During purine catabolism, both conversions of Gr to G and of Xant to Xan are reversible. Decreased ratios of product to precursor suggested a shift favorable to Xant production from Xan, resulting in decreased UA levels in the FENNS. Specifically, the reduced UA/Gr ratio was nearly normalized after 4 weeks of antipsychotic treatment. In addition, there are tightly correlated precursor and product relationships within purine pathways; although some of these correlations persist across disease or medication status, others appear to be lost among FENNS. Taken together, these results suggest that the potential for steady formation of antioxidant UA from purine catabolism is altered early in the course of illness.
dc.format.extent e9508 - ?
dc.language ENG
dc.language.iso en_US en_US
dc.relation.ispartof PLoS One
dc.relation.isversionof 10.1371/journal.pone.0009508
dc.subject Adolescent
dc.subject Adult
dc.subject Antipsychotic Agents
dc.subject Case-Control Studies
dc.subject Diet
dc.subject Female
dc.subject Guanosine
dc.subject Homeostasis
dc.subject Humans
dc.subject Hypoxanthine
dc.subject Male
dc.subject Metabolism
dc.subject Oxidation-Reduction
dc.subject Oxidative Stress
dc.subject Purines
dc.subject Ribonucleosides
dc.subject Schizophrenia
dc.subject Smoking
dc.subject Uric Acid
dc.title Homeostatic imbalance of purine catabolism in first-episode neuroleptic-naïve patients with schizophrenia.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2010-3-3 en_US
duke.description.endpage e9508 en_US
duke.description.issue 3 en_US
duke.description.startpage e9508 en_US
duke.description.volume 5 en_US
dc.relation.journal Plos One en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20209081
pubs.issue 3
pubs.organisational-group /Duke
pubs.organisational-group /Duke/Institutes and Provost's Academic Units
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers
pubs.organisational-group /Duke/Institutes and Provost's Academic Units/University Institutes and Centers/Duke Institute for Brain Sciences
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Cardiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Psychiatry & Behavioral Sciences
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Psychiatry & Behavioral Sciences/Psychiatry & Behavioral Sciences, Behavioral Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Psychiatry & Behavioral Sciences/Psychiatry & Behavioral Sciences, Translational Neuroscience
pubs.publication-status Published online
pubs.volume 5
dc.identifier.eissn 1932-6203

Files in this item

This item appears in the following Collection(s)

Show simple item record