title: Protective effect of selenium on gentamicin-induced oxidative stress and nephrotoxicity in rats.
abstract: Gentamicin (GM) is a widely used antibiotic against serious, life-threatening infections, but its usefulness is limited by the development of nephrotoxicity. The present study was designed to determine the protective effect of selenium (Se) in GM-induced nephrotoxicity in rats. Experiments were done on 32 adult Wistar rats divided into four groups of 8 animals each. The GM group received gentamicin (100 mg/kg), whereas the GM+Se group received the same dose of GM and selenium (1 mg/kg) by intraperitoneal (i.p.) injections on a daily basis. Animals in the Se group, serving as a positive control, received only selenium (1 mg/kg) and the control group received saline (1 mL/day), both given i.p. All groups were treated during 8 consecutive days. Quantitative evaluation of GM-induced structural alterations and degree of functional alterations in the kidneys were performed by histopathological and biochemical analyses in order to determine potential beneficial effects of selenium coadministration with GM. GM was observed to cause a severe nephrotoxicity, which was evidenced by an elevation of serum urea and creatinine levels. The significant increases in malondialdehyde levels and protein carbonyl groups indicated that GM-induced tissue injury was mediated through oxidative reactions. On the other hand, simultaneous selenium administration protected kidney tissue against oxidative damage and the nephrotoxic effect caused by GM treatment. Exposure to GM caused necrosis of tubular epithelial cells. Necrosis of tubules was found to be prevented by selenium pretreatment.   The results from our study indicate that selenium supplementation attenuates oxidative-stress-associated renal injury by reducing oxygen free radicals and lipid peroxidation in GM-treated rats.
authors.affiliation: Departments of Physiology, University of Nis, Nis, Serbia. pavleus@gmail.com
authors.forename: Pavle
authors.initials: P
authors.lastname: Randjelovic
authors.forename: Slavimir
authors.initials: S
authors.lastname: Veljkovic
authors.forename: Nenad
authors.initials: N
authors.lastname: Stojiljkovic
authors.forename: Ljubinka
authors.initials: L
authors.lastname: Velickovic
authors.forename: Dusan
authors.initials: D
authors.lastname: Sokolovic
authors.forename: Milan
authors.initials: M
authors.lastname: Stoiljkovic
authors.forename: Ivan
authors.initials: I
authors.lastname: Ilic
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000633:toxicity*; D003404:Creatinine / Q000097:blood; D005839:Gentamicins / Q000633:toxicity*; D006651:Histocytochemistry; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018038:Sodium Selenite / Q000494:pharmacology*; D014508:Urea / Q000097:blood
chemical_list: D000900:Anti-Bacterial Agents; D005839:Gentamicins; D008315:Malondialdehyde; D014508:Urea; D003404:Creatinine; D018038:Sodium Selenite