Εμφάνιση απλής εγγραφής

dc.creatorTsamouri M.-M., Rapti M., Kouka P., Nepka C., Tsarouhas K., Soumelidis A., Koukoulis G., Tsatsakis A., Kouretas D., Tsitsimpikou C.en
dc.date.accessioned2023-01-31T10:11:25Z
dc.date.available2023-01-31T10:11:25Z
dc.date.issued2017
dc.identifier10.1016/j.fct.2017.07.058
dc.identifier.issn02786915
dc.identifier.urihttp://hdl.handle.net/11615/79842
dc.description.abstractContrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury as a result of iodinated contrast-media use for diagnostic purposes. Pathophysiology remains unclear. In the present study iopromide was administered to New Zealand white rabbits without any prior intervention. Oxidative stress was assessed in blood and tissue level at three anatomical kidney areas (medullary, cortical, juxtamedullary). Histopathological evaluation was also performed. Serum creatinine and urea increased in the CIN groups over 25% at two hours after administration and returned to baseline at 48 h. In kidney tissues, a significant reduction (40%) of catalase in renal cortexes of the CIN groups was observed. Necrosis and tubular vacuolization was also noted that correlated with urea and creatinine levels. Lipid peroxidation decreased at 10 h after administration (>45%) and remained low even at 48 h. Plasma protein carbonyls were significantly increased (67%) in 2 h and dropped later. Serum levels of creatinine and urea at 24 and 48 h significantly correlated with the Total Antioxidant Activity and lipid peroxidation, respectively. Oxidative stress is shown to be involved in CIN development in the rabbit, with more pronounced effects to be confined to the cortex and outer stripe of the outer medulla. © 2017en
dc.language.isoenen
dc.sourceFood and Chemical Toxicologyen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85026800431&doi=10.1016%2fj.fct.2017.07.058&partnerID=40&md5=b19cb9efdea05c0c5945829b4e86e162
dc.subjectcatalaseen
dc.subjectcreatinineen
dc.subjectiopromideen
dc.subjectplasma proteinen
dc.subjectureaen
dc.subjectbiological markeren
dc.subjectcontrast mediumen
dc.subjectcreatinineen
dc.subjectiohexolen
dc.subjectureaen
dc.subjectanimal experimenten
dc.subjectanimal modelen
dc.subjectanimal tissueen
dc.subjectArticleen
dc.subjectblood analysisen
dc.subjectcontrast induced nephropathyen
dc.subjectcontrolled studyen
dc.subjectcreatinine blood levelen
dc.subjecthistopathologyen
dc.subjectkidney cortexen
dc.subjectkidney medullaen
dc.subjectkidney necrosisen
dc.subjectkidney tissueen
dc.subjectlipid peroxidationen
dc.subjectmaleen
dc.subjectNew Zealand rabbiten
dc.subjectnonhumanen
dc.subjectoxidative stressen
dc.subjectpathogenesisen
dc.subjecturea blood levelen
dc.subjectanalogs and derivativesen
dc.subjectanimalen
dc.subjectblooden
dc.subjectchemically induceden
dc.subjectdrug effectsen
dc.subjectkidneyen
dc.subjectkidney diseaseen
dc.subjectLeporidaeen
dc.subjectmetabolismen
dc.subjectoxidation reduction reactionen
dc.subjectoxidative stressen
dc.subjectpathologyen
dc.subjectrandomizationen
dc.subjectAnimalsen
dc.subjectBiomarkersen
dc.subjectContrast Mediaen
dc.subjectCreatinineen
dc.subjectIohexolen
dc.subjectKidneyen
dc.subjectKidney Diseasesen
dc.subjectMaleen
dc.subjectOxidation-Reductionen
dc.subjectOxidative Stressen
dc.subjectRabbitsen
dc.subjectRandom Allocationen
dc.subjectUreaen
dc.subjectElsevier Ltden
dc.titleHistopathological evaluation and redox assessment in blood and kidney tissues in a rabbit contrast-induced nephrotoxicity modelen
dc.typejournalArticleen


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