title: Seleno L-methionine acts on cyclophosphamide-induced kidney toxicity.
abstract: The anticancer drug cyclophosphamide (CP) has nephrotoxic effects besides its urotoxicity, which both in turn limit its clinical utility. The nephrotoxicity of CP is less common compared to its urotoxicity, and not much importance has been given for the study of mechanism of CP-induced nephrotoxicity so far. Overproduction of reactive oxygen species (ROS) during inflammation is one of the reasons of the kidney injury. Selenoproteins play crucial roles in regulating ROS and redox status in nearly all tissues; therefore, in this study, the nephrotoxicity of CP and the possible protective effects of seleno L-methionine (SLM) on rat kidneys were investigated. Forty-two Sprague-Dawley rats were equally divided into six groups of seven rats each. The control group received saline, and other rats were injected with CP (100 mg/kg), SLM (0.5 or 1 mg/kg), or CP + SLM intraperitoneally. Malondialdehyde (MDA) and glutathione (GSH) levels in kidney homogenates of rats were measured, and kidney tissues were examined under the microscope. CP-treated rats showed a depletion of renal GSH levels (28% of control), while CP + SLM-injected rats had GSH values close to the control group. MDA levels increased 36% of control following CP administration, which were significantly decreased after SLM treatment. Furthermore, these biochemical results were supported by microscopical observations. In conclusion, the present study not only points to the therapeutic potential of SLM in CP-induced kidney toxicity but also indicates a significant role for ROS and their relation to kidney dysfunction.
authors.affiliation: Faculty of Arts and Science, Department of Biology, Eskisehir Osmangazi University, Eskisehir, Turkey. aayhanci@ogu.edu.tr
authors.forename: Adnan
authors.initials: A
authors.lastname: Ayhanci
authors.forename: Sibel
authors.initials: S
authors.lastname: Günes
authors.forename: Varol
authors.initials: V
authors.lastname: Sahinturk
authors.forename: Sila
authors.initials: S
authors.lastname: Appak
authors.forename: Ruhi
authors.initials: R
authors.lastname: Uyar
authors.forename: Mustafa
authors.initials: M
authors.lastname: Cengiz
authors.forename: Yilmaz
authors.initials: Y
authors.lastname: Altuner
authors.forename: Suzan
authors.initials: S
authors.lastname: Yaman
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects / Q000627:therapeutic use / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology*; D003520:Cyclophosphamide / Q000009:adverse effects / Q000627:therapeutic use / Q000633:toxicity*; D005260:Female; D005978:Glutathione / Q000097:blood; D007668:Kidney / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000633:toxicity; D012015:Reference Standards; D012645:Selenomethionine / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D000975:Antioxidants; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D003520:Cyclophosphamide; D012645:Selenomethionine; D005978:Glutathione