title: Radiation-induced chronic oxidative renal damage can be reduced by amifostine.
abstract: In the current study, amifostine is evaluated for its radioprotective role in serum and kidney tissue by oxidative (malondialdehyde-MDA, advanced oxidation protein product-AOPP) and antioxidative markers (catalase, glutathione-GSH, free-thiols-F-SH). Thirty Wistar albino 3-4 months old, female rats, were randomly divided into Group I (n = 10): Control, Group II (n = 10): Irradiation-alone, Group III (n = 10): Amifostine before irradiation. In Group II and III, right kidneys of the rats were irradiated with a single dose of 6 Gy using a 60Co treatment unit. Rats in Group III received 200 mg/kg amifostine intraperitoneally, 30 min prior to irradiation. Following sacrification at 24th week, blood and kidney tissue samples were collected. Statistical analysis was done by One-way ANOVA, Post hoc Bonferroni, Dunnett T3, and Mann-Whitney U tests. Administration of amifostine significantly decreased the serum AOPP and MDA levels when compared to the irradiation-only group (P = 0.004, P = 0.006; respectively). Also amifostine significantly increased serum catalase activities and GSH levels, when given 30 min prior to irradiation (P = 00.02, P = 0.000; respectively). In the kidney tissue, administration of amifostine significantly decreased AOPP and MDA levels (P = 0.002, P = 0.016; respectively). Tissue GSH activity was increased following amifostine administration (P = 0.001). There was no statistically significant result on histopathological evaluation. Amifostine may reduce radiation-induced nephropathy by inhibiting chronic oxidative stress. Biomarkers of oxidative stress in serum and kidney tissue may be used for evaluation of the radiation-induced nephropathy.
authors.affiliation: Department of Radiation Oncology, Trakya University Faculty of Medicine, 22030 Edirne, Turkey. rusencosar@yahoo.com
authors.forename: Rusen
authors.initials: R
authors.lastname: Cosar
authors.forename: Vuslat
authors.initials: V
authors.lastname: Yurut-Caloglu
authors.forename: Sevgi
authors.initials: S
authors.lastname: Eskiocak
authors.forename: Alaattin
authors.initials: A
authors.lastname: Ozen
authors.forename: Semsi
authors.initials: S
authors.lastname: Altaner
authors.forename: Kamuran
authors.initials: K
authors.lastname: Ibis
authors.forename: Nesrin
authors.initials: N
authors.lastname: Turan
authors.forename: Bengu
authors.initials: B
authors.lastname: Denizli
authors.forename: Cem
authors.initials: C
authors.lastname: Uzal
authors.forename: Mert
authors.initials: M
authors.lastname: Saynak
authors.forename: Sule
authors.initials: S
authors.lastname: Parlar
authors.forename: Murat
authors.initials: M
authors.lastname: Caloglu
authors.forename: Burcu
authors.initials: B
authors.lastname: Uregen
authors.forename: Zafer
authors.initials: Z
authors.lastname: Kocak
mesh_terms: D004999:Amifostine / Q000627:therapeutic use*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002908:Chronic Disease; D003037:Cobalt Radioisotopes / Q000009:adverse effects*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007674:Kidney Diseases / Q000209:etiology* / Q000517:prevention & control*; D008315:Malondialdehyde / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D011836:Radiation Tolerance / Q000187:drug effects*; D011837:Radiation-Protective Agents / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D003037:Cobalt Radioisotopes; D011837:Radiation-Protective Agents; D008315:Malondialdehyde; D002374:Catalase; D005978:Glutathione; D004999:Amifostine