Amikacin induced renal damage and the role of the antioxidants on neonatal rats

dc.contributor.authorKara, Aslihan
dc.contributor.authorCetin, Hasan
dc.contributor.authorOktem, Faruk
dc.contributor.authorCiris, Ibrahim Metin
dc.contributor.authorAltuntas, Irfan
dc.contributor.authorKaya, Selcuk
dc.date.accessioned2026-08-12T17:48:46Z
dc.date.issued2016
dc.departmentFırat Üniversitesi
dc.description.abstractAmikacin (AK) is frequently used on the treatment of Gram-negative infections on neonates, but its usage is restricted because of nephrotoxicity. In this study, on neonatal rats, we aimed to investigate the effects of erythropoietin and vitamin E on AK induced nephrotoxicity. A total of 35 newborn Wistar Albino rats were divided into four groups: (1) injected with saline (serum physiological was administered to placebo controls), (2) injected with AK (1200mg/kg), (3) injected with AK+vitamin E (150mg/kg), (4) injected with AK+erythropoietin (EPO) (300IU/kg/day). In renal tissue, AK levels were significantly high in all groups except the control. Tissue malondialdehyde (MDA) and nitric oxide (NO) levels were statistically higher in AK -treated group than the control. MDA and NO levels were significantly decreased with the administration of vitamin E and EPO. Glutathione peroxidase (GPX) levels were statistically low in AK group compared with the controls. The levels of GPX, in vitamin E group, were increased significantly. However, superoxide dismutase and catalase levels were not significantly different in none of the groups. Insulin-like growth factor-1 values in AK, EPO and vitamin E groups were significantly higher than the control group. Histomorphological changes such as tubular epithelial necrosis were seen in AK treated group. Histopathological improvements observed with EPO and vitamin E administration. AK nephrotoxicity is related to oxidative stress and is supported with biochemical and histopathological findings. Vitamin E and EPO, as antioxidants, can be useful renoprotective agents for ameliorating AK induced nephrotoxicity in neonates.
dc.description.sponsorshipSuleyman Demirel University [1456-TU-06]
dc.description.sponsorshipThis work financially supported by the Suleyman Demirel University Research Fund (Project No: 1456-TU-06).
dc.identifier.doi10.3109/0886022X.2016.1155393
dc.identifier.endpage677
dc.identifier.issn0886-022X
dc.identifier.issn1525-6049
dc.identifier.issue5
dc.identifier.orcid0000-0003-4410-0444
dc.identifier.orcid0000-0002-8637-6345
dc.identifier.pmid26982694
dc.identifier.scopus2-s2.0-84961213844
dc.identifier.scopusqualityQ2
dc.identifier.startpage671
dc.identifier.urihttps://doi.org/10.3109/0886022X.2016.1155393
dc.identifier.urihttps://hdl.handle.net/11508/61549
dc.identifier.volume38
dc.identifier.wosWOS:000378756000003
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofRenal Failure
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260511
dc.subjectAmikacin
dc.subjecterythropoietin
dc.subjectneonatal rats
dc.subjectoxidative injury
dc.subjectvitamin E
dc.titleAmikacin induced renal damage and the role of the antioxidants on neonatal rats
dc.typeArticle

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