Linked Life Data

18448592

Source:http://linkedlifedata.com/resource/pubmed/id/18448592

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-8-4
pubmed:abstractText
Hyperoxaluric kidneys show an impaired diuretic response to acute infusion of L-arginine. In this study, we examined the chronic effect of l-arginine supplementation on CaOx crystal formation in hyperoxaluric rat kidneys. Eight groups were tested: control (received drinking water), L group (received L-arginine, 0.6%), LN group [received NG-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg)], L + LN group (received L-arginine + l-NAME), HP group [received hydroxyl-L-proline (HP, 5%) mixed with chow to induce hyperoxaluria], L + HP group (received HP + L-arginine), HP + LN group, and L + HP + LN group. The duration was 42 days, and each group had eight animals. Urinary biochemistry and renal CaOx amounts were measured, as well as renal expressions of nitric oxide synthase (NOS) isoforms and NAD(P)H oxidase. The distribution of inducible NOS (iNOS), NAD(P)H oxidase, ED1-positive cells, and nitrotyrosine was examined by immunohistochemical and immunofluorescence studies, whereas superoxide production from the kidneys was examined by fluorescence spectrometric assay. Compared with the HP group, the L + HP group had excessive CaOx crystal accumulation and enhanced endothelial NOS (eNOS), iNOS, and NAD(P)H oxidase protein expression in the kidney. Urinary excretion of nitrotyrosine was markedly increased. Increased superoxide formation in the L + HP kidney was derived from NAD(P)H oxidase and uncoupled eNOS, and increased nitrotyrosine formation might derive from iNOS and ED1-positive cells that gathered around the CaOx crystals. L-NAME cotreatment (L + HP + LN group) reduced renal oxidative nitrosative stress and tubular damage, which were induced by L + HP. The results showed that chronic l-arginine treatment to the hyperoxaluric kidney with massive CaOx crystal deposition may have a toxic effect by enhancing intrarenal oxidative and nitrosative stress.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
295
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F388-96
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:18448592-Animals, pubmed-meshheading:18448592-Arginine, pubmed-meshheading:18448592-Calcium Oxalate, pubmed-meshheading:18448592-Crystallization, pubmed-meshheading:18448592-Disease Models, Animal, pubmed-meshheading:18448592-Dose-Response Relationship, Drug, pubmed-meshheading:18448592-Enzyme Inhibitors, pubmed-meshheading:18448592-Hydroxyproline, pubmed-meshheading:18448592-Hyperoxaluria, pubmed-meshheading:18448592-Kidney, pubmed-meshheading:18448592-Male, pubmed-meshheading:18448592-NADPH Oxidase, pubmed-meshheading:18448592-NG-Nitroarginine Methyl Ester, pubmed-meshheading:18448592-Nitric Oxide Synthase, pubmed-meshheading:18448592-Nitric Oxide Synthase Type II, pubmed-meshheading:18448592-Nitric Oxide Synthase Type III, pubmed-meshheading:18448592-Oxidative Stress, pubmed-meshheading:18448592-Rats, pubmed-meshheading:18448592-Rats, Wistar, pubmed-meshheading:18448592-Reactive Oxygen Species, pubmed-meshheading:18448592-Superoxides
pubmed:year
2008
pubmed:articleTitle
Chronic L-arginine administration increases oxidative and nitrosative stress in rat hyperoxaluric kidneys and excessive crystal deposition.
pubmed:affiliation
Department of Urology, National Taiwan University Hospital, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't