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    Cytoprotective effects of amifostine, ascorbic acid and N-acetylcysteine against methotrexate-induced hepatotoxicity in rats
    (Baishideng Publishing Group Inc, 2014) Akbulut, Sami; Elbe, Hulya; Eris, Cengiz; Dogan, Zumrut; Toprak, Gulten; Otan, Emrah; Erdemli, Erman
    AIM: To investigate the potential role of oxidative stress and the possible therapeutic effects of N-acetyl cysteine (NAC), amifostine (AMF) and ascorbic acid (ASC) in methotrexate (MTX)-induced hepatotoxicity. METHODS: An MTX-induced hepatotoxicity model was established in 44 male Sprague Dawley rats by administration of a single intraperitoneal injection of 20 mg/kg MTX. Eleven of the rats were left untreated (Model group; n = 11), and the remaining rats were treated with a 7-d course of 50 mg/kg per day NAC (MTX + NAC group; n = 11), 50 mg/kg per single dose AMF (MTX + AMF group; n = 11), or 10 mg/kg per day ASC (MTX + ASC group; n = 11). Eleven rats that received no MTX and no treatments served as the negative control group. Structural and functional changes related to MTX- and the various treatments were assessed by histopathological analysis of liver tissues and biochemical assays of malondialdehyde (MDA), superoxide dismutase (SOD), catalase, glutathione (GSH) and xanthine oxidase activities and of serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin. RESULTS: Exposure to MTX caused structural and functional hepatotoxicity, as evidenced by significantly worse histopathological scores [median (range) injury score: control group: 1 (0-3) vs 7 (6-9), p = 0.001] and significantly higher MDA activity [409 (352-466) nmol/g vs 455.5 (419-516) nmol/g, p < 0.05]. The extent of MTX-induced perturbation of both parameters was reduced by all three cytoprotective agents, but only the reduction in hepatotoxicity scores reached statistical significance [4 (3-6) for NAC, 4.5 (3-5) for AMF and 6 (5-6) for ASC; p = 0.001, p = 0.001 and p < 0.005 vs model group respectively]. Exposure to MTX also caused a significant reduction in the activities of GSH and SOD antioxidants in liver tissues [control group: 3.02 (2.85-3.43) mu mol/g and 71.78 (61.88-97.81) U/g vs model group: 2.52 (2.07-3.34) mu mol/g and 61.46 (58.27-67.75) U/g, p < 0.05]; however, only the NAC treatment provided significant increases in these antioxidant enzyme activities [3.22 (2.54-3.62) mu mol/g and 69.22 (61.13-100.88) U/g, p < 0.05 and p < 0.01 vs model group respectively]. CONCLUSION: MTX-induced structural and functional damage to hepatic tissues in rats may involve oxidative stress, and cytoprotective agents (NAC > AMF > ASC) may alleviate MTX hepatotoxicity. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
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    Effects of antioxidant agents against cyclosporine-induced hepatotoxicity
    (Academic Press Inc Elsevier Science, 2015) Akbulut, Sami; Elbe, Hulya; Eris, Cengiz; Dogan, Zumrut; Toprak, Gulten; Yalcin, Erhan; Otan, Emrah
    Background: To investigate the potential protective antioxidant role of ursodeoxycholic acid (UDCA), melatonin, and allopurinol treatment in cyclosporine (CsA)-induced hepatotoxicity. Methods: Hepatotoxicity was established in Sprague-Dawley rats by daily administration of CsA. Treatment groups were additionally administered UDCA, melatonin, or allopurinol treatments. Rats that received no CsA and no treatments served as a control group. Liver samples from each group were examined by histopathologic analysis to determine the effects of CsA treatment on liver morphology. Biochemical assays were also used to determine the effect of CsA treatment on liver function, in the presence or absence of UDCA, melatonin, or allopurinol. Results: CsA treatment induced hepatotoxicity, resulting in sinusoidal dilatation, congestion, infiltration, hydropic degeneration, and loss of glycogen storage in the liver. From a molecular perspective, the CsA treatment increased levels of malondialdehyde (MDA) levels, decreased levels of reduced glutathione and xanthine oxidase, and decreased activities of superoxide dismutase and catalase. The CsA treatment also resulted in decreased serum total antioxidant capacity, whereas alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bilirubin levels, and total oxidant status were increased. Treatment with UDCA, melatonin, or allopurinol reduced the CsA-induced histopathologic changes, as compared with CsA-treated samples. In addition, UDCA, melatonin, or allopurinol treatment mitigated the CsA-induced effects on glutathione and MDA levels, and on superoxide dismutase and catalase activities, as well as reduced the CsA-mediated perturbations in serum levels of total antioxidant capacity, total oxidant status, and alkaline phosphatase. Conclusions: UDCA, allopurinol, and melatonin may each help to protect against CsA-induced damage to liver tissues, possibly through effects on the antioxidant system. (C) 2015 Elsevier Inc. All rights reserved.
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    Hydatid Disease of the Spleen: Single-Center Experience and a Brief Literature Review
    (Springer, 2013) Akbulut, Sami; Sogutcu, Nilgun; Eris, Cengiz
    The aim of this study was to discuss the management of patients with splenic hydatid cyst (SHC) and to provide a review of the literature in this field. The outcomes of patients surgically treated for SHC at the Diyarbakir Education and Research Hospital (DERH) between January 2006 and May 2013 were assessed by retrospectively reviewing demographic, radiological, and clinical data. In addition, the outcome profiles of these patients were compared to the overall outcomes of surgically treated SHC cases reported in the literature. Relevant case series (a parts per thousand yen4 cases) were identified by searching the PubMed, Medline, and Google Scholar databases for publications from 1990 to May 2013 in English or Turkish languages. Nine patients with SHC received surgical treatment at DERH (age range, 18-53 years old; mean, 36.9 +/- 11.8; female/male, 7/2), including five (55.6 %) primary SHC and four (44.4 %) secondary (100 % liver) SHC cases. Two patients had previous SHC surgery. Seven patients received albendazole therapy, both preoperative (10-21 days) and postoperative (10-42 days) periods. All patients received vaccination, either preoperative (n = 4) or postoperative (n = 5). Six patients underwent splenectomy and three underwent splenectomy with partial cystectomy and omentopexy, and no patient experienced SHC recurrence during follow-up (1-60 months). The literature review identified 27 full-text articles representing 333 surgically treated SHC cases, among which 60.5 % had primary SHC and 39.5 % had secondary SHC. Two hundred thirty of 333 patients underwent splenectomy, 81 underwent spleen-sparing surgery, and 17 underwent puncture, aspiration, injection, and reaspiration. The remaining five patients were not operated for various reasons. We found no significant difference in recurrence rates between splenectomy and spleen-sparing surgery, either in our patient cohort or among cases reported in the literature. Nevertheless, we cannot make any solid recommendations for either procedure based on these results, as the studies were largely retrospective.