Protective role of aminoguanidine on gentamicin induced acute renal failure in rats

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dc.authorid9217en_US
dc.contributor.authorPolat, Alaadin
dc.contributor.authorParlakpınar, Hakan
dc.contributor.authorTaşdemir, Seda
dc.contributor.authorÇolak, Cemil
dc.contributor.authorVardı, Nigar
dc.contributor.authorUçar, Muharrem
dc.contributor.authorEmre, Mehmet Hanifi
dc.contributor.authorAcet, Hacı Ahmet
dc.date.accessioned2017-08-22T07:12:39Z
dc.date.available2017-08-22T07:12:39Z
dc.date.issued2006
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe toxicity of aminoglycosides including gentamicin (GEN), the most widely used drug in this category, is believed to be related to the generation of reactive oxygen species (ROS) in the kidney. Aminoguanidine (AG) is known as an effective antioxidant and its free radical scavenger effects may protect GEN-induced acute renal failure (ARF). Therefore, this study was focused on investigating the possible protective effect of AG against GENinduced nephrotoxicity in an in vivo rat model. We investigated the effects of AG on GENinduced changes in renal tissue malondialdehyde (MDA) levels; nitric oxide (NO) generation; glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities; glutathione (GSH) content; serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined using light microscopy. GEN administration to control group rats increased renal MDA and NO levels but decreased GSH-Px, SOD, CAT activities and GSH content. AG administration with GEN injection resulted in significantly decreased MDA, NO generation and increased GSH-Px, SOD, CAT activities and GSH content when compared with GEN alone. Serum levels of Cr and BUN significantly increased as a result of nephrotoxicity. Also, AG significantly decreased Cr and BUN levels. Morphological changes in the kidney, including tubular necrosis, intracellular edema, glomerular and basement membrane alterations were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of AG reduced the GEN-induced kidney damage. We propose that AG acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level.en_US
dc.identifier.citationPolat, A. Parlakpınar, H. Taşdemir, S. Çolak, C. Vardı, N. Uçar, M. Emre, M. H. Acet, H. A. (2006). Protective role of aminoguanidine on gentamicin induced acute renal failure in rats. Acta Histochemica. 108(5), 365–371.en_US
dc.identifier.doi10.1016/j.acthis.2006.06.005en_US
dc.identifier.endpage371en_US
dc.identifier.issn00651281
dc.identifier.issue5en_US
dc.identifier.startpage365en_US
dc.identifier.urihttps://hdl.handle.net/11616/7668
dc.identifier.volume108en_US
dc.language.isoenen_US
dc.publisherActa Histochemicaen_US
dc.relation.ispartofActa Histochemicaen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAminoguanidineen_US
dc.subjectGentamicinen_US
dc.subjectReactive oxygen radicalsen_US
dc.subjectRenal injuryen_US
dc.subjectRaten_US
dc.titleProtective role of aminoguanidine on gentamicin induced acute renal failure in ratsen_US
dc.typeArticleen_US

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