Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

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    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, Sıla
    The 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: 16
    Citation - Scopus: 17
    Protective Effect of Zinc on Cyclophosphamide-Induced Hematoxicity and Urotoxicity
    (Humana Press, 2008) Ayhancı, Adnan; Uyar, Ruhi; Aral, Erinç; Kabadere, Selda; Appak, Sıla
    Cyclophosphamide (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.