Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
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Other Erratum: Protective Effect of Zinc on Cyclophosphamide-Induced Hematoxicity and Urotoxicity: (biol Trace Elem Res (2008) 126 (186-193) Doi 10.1007/S12011-008-8189-5)(Humana Press, 2009) Ayhancı, Adnan; Uyar, Ruhi; Aral, Erinç; Kabadere, Selda; Appak, SılaThe original version of this article unfortunately contained a mistake. The Materials and Methods section should include last paragraph. Section “Materials and Methods”, inclusion of the last paragraph should read: Only the groups which had CY treatment alone were killed 3 days after the CY injection. For the groups having Cy+ZnCl2 , ZnCl2 administration was started three days earlier than the CY administration and continued till the end of the experiment (6 days). On the fourth day the animals were weighed again, relative doses of CY were estimated and CY+ZnCl2 was administered together. On the seventh day blood samples were collected, bone marrow and the urinary bladders of the animals were resected under anesthesia. Also, the first three affiliations were incorrect. The correct information is given below.Article Citation - WoS: 11Citation - Scopus: 13Protective Effect of Seleno-L on Cyclophosphamide-Induced Urinary Bladder Toxicity in Rats(Humana Press, 2010) Ayhancı, Adnan; Yaman, Suzan; Şahintürk, Varol; Uyar, Ruhi; Bayramoğlu, Gökhan; Şentürk, Hakan; Altuner, Yılmaz; Appak, Sıla; Güneş, SibelCyclophosphamide (CP) is a widely used antineoplastic drug, which could cause toxicity of the normal cells due to its toxic metabolites. Its urotoxicity may cause dose-limiting side effects like hemorrhagic cystitis. Overproduction of reactive oxygen species (ROS) during inflammation is one of the reasons of the urothelial injury. Selenoproteins play crucial roles in regulating ROS and redox status in nearly all tissues; therefore, in this study, the urotoxicity of CP and the possible protective effects of seleno-l-methionine (SLM) on urinary bladder of rats were investigated. Intraperitoneal (i.p.) administration of 50, 100, or 150 mg/kg CP induced cystitis, in a dose-dependent manner, as manifested by marked congestion, edema and extravasation in rat urinary bladder, a marked desquamative damage to the urothelium, severe inflammation in the lamina propria, focal erosions, and polymorphonuclear (PMN) leukocytes associated with occasional lymphocyte infiltration determined by macroscopic and histopathological examination. In rat urinary bladder tissue, a significant decrease in the endogenous antioxidant compound glutathione, and elevation of lipid peroxidation were also noted. Pretreatment with SLM (0.5 or 1 mg/kg) produced a significant decrease in the bladder edema and caused a marked decrease in vascular congestion and hemorrhage and a profound improvement in the histological structure. Moreover, SLM pretreatment decreased lipid peroxide significantly in urinary bladder tissue, and glutathione content was greatly restored. These results suggest that SLM offers protective effects against CP-induced urinary bladder toxicity and could be used as a protective agent against the drug toxicity. © 2009 Humana Press Inc.Article Citation - WoS: 51Citation - Scopus: 55Seleno L-Methionine Acts on Cyclophosphamide-Induced Kidney Toxicity(Humana Press, 2010) Ayhancı, Adnan; Güneş, Sibel; Şahintürk, Varol; Appak, Sıla; Uyar, Ruhi; Cengiz, Mustafa; Altuner, Yılmaz; Yaman, SuzanThe 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. © Humana Press Inc. 2009.Article Citation - WoS: 16Citation - Scopus: 17Protective Effect of Zinc on Cyclophosphamide-Induced Hematoxicity and Urotoxicity(Humana Press, 2008) Ayhancı, Adnan; Uyar, Ruhi; Aral, Erinç; Kabadere, Selda; Appak, SılaCyclophosphamide (CP) is widely used for the treatment of neoplastic diseases; however, its toxicity causes dose-limiting side effects. Zinc (Zn) is an essential trace element and has important biological functions that control many cell processes including DNA synthesis, normal growth, reproduction, fetal development, bone formation, and wound healing. Therefore, the toxicity of CP and the possible protective effect of Zn on blood cells, bone marrow, and bladder of rat were investigated in this study. Intraperitoneal administration of 50, 100, or 150 mg/kg CP for 3 days caused, in a dose-dependent manner, reductions in the number of leukocytes, thrombocytes, and bone marrow nucleated cells and a serious urotoxicity. To explore whether CP-induced damages could be prevented by Zn, other groups of rats were pretreated with 4 or 8 mg/kg ZnCl2 intraperitoneally for 3 days then challenged with respective doses of CP plus ZnCl2 on day 4 for three more days. The results indicated that treatment of rats with Zn could dose-dependently alleviate CP-induced toxicities on blood cells, bone marrow cells, and urinary bladder. We suggest that Zn could be a potentially effective drug in the prevention of CP-related hematoxicity and urotoxicity.