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    Cabazitaxel causes a dose-dependent central nervous system toxicity in rats
    (Elsevier, 2016) Karavelioglu, Ergun; Gonul, Yucel; Aksit, Hasan; Boyaci, Mehmet Gazi; Karademir, Mustafa; Simsek, Nejdet; Guven, Mustafa
    Background: Chemotherapeutic agents may lead to serious neurological side effects, which in turn can deteriorate the quality of life and cause dose limiting. Direct toxic effect or metabolic derangement of chemotherapeutic agents may cause these complications. Cabazitaxel is a next generation semi-synthetic taxane derivative, which is effective in both preclinical models of human tumors sensitive or resistant to chemotherapy and in patients with progressive prostate cancer despite docetaxel treatment. Aim: The primary aim of this study was to investigate the central nervous system toxicity of Cabazitaxel. Secondary aim was to investigate the safety dose of Cabazitaxel for the central nervous system. Methods: A total of 24 adult male Wistar-Albino rats were equally and randomly divided into four groups as follows: group 1 (Controls), group 2 (Cabazitaxel 0.5 mg/kg), group 3 (Cabazitaxel 1.0 mg/kg) and group 4 (Cabazitaxel 1.5 mg/kg). Cabazitaxel (Jevtana, Sanofi-Aventis USA) was intraperitoneally administered to groups 2, 3 and 4 at 05, 1.0 and 1.5 mg/kg (body-weight/week) doses, respectively for four consecutive weeks. Beside this, group 1 received only i.p. saline at the same volume and time. At the end of the study, animals were sacrificed and bilateral brain hemispheres were removed for biochemical, histopathological and immunohistochemical examinations. Results: Intraperitoneal administration of Cabazitaxel has exerted neurotoxic effect on rat brain. We have observed that biochemical and immunohistochemical results became worse in a dose dependent manner. Conclusion: Our findings have suggested that Cabazitaxel may be a neurotoxic agent and can trigger apoptosis in neuron cells especially at high doses. (C) 2015 Elsevier B.V. All rights reserved.
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    Does protocatechuic acid, a natural antioxidant, reduce renal ischemia reperfusion injury in rats?
    (Turkish Assoc Trauma Emergency Surgery, 2017) Yuksel, Melih; Yildar, Murat; Basbug, Murat; Cavdar, Faruk; Cikman, Oztekin; Aksit, Hasan; Aslan, Figen
    BACKGROUND: Protocatechuic acid (PCA), which has antioxidant property, is a simple phenolic compound commonly found in many plants, vegetables, and fruits, notably in green tea and almonds. Present study was an investigation of the effects of PCA on rat kidney with ischemia/reperfusion (IR) injury. METHODS: Sprague-Dawley rats were randomly divided into 4 groups: (1) Sham, (2) Renal IR, (3) Renal IR+ Vehicle, and (4) Renal IR+ PCA. Renal reperfusion injury was induced by clamping renal pedicle for 45 minutes after right nephrectomy was performed, followed by reperfusion for 3 hours. Dose of 80 mg/kg PCA was intraperitoneally administered to 1 group immediately before renal ischemia; 33% polyethylene glycol was used as vehicle. Total antioxidant status (TAS), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 levels were measured in blood and kidney tissue samples taken from sacrificed rats. Kidney tissue samples were examined and scored histopathologically. Terminal deoxynucleotidyltransferase-mediated dUTP digoxigenin nick end labeling assay method was used to detect apoptotic cells. RESULTS: It was found that PCA significantly reduced serum MDA, TNF-alpha, and kidney MDA levels, while it increased serum and kidney TAS and SOD levels. Histopathological scores were significantly higher for the group given PCA. CONCLUSION: PCA reduced oxidative stress and can be used as an effective agent in treatment of renal IR injury.
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    Effect of different doses of 2aEuroaminoethoxydiphenyl borate on intestinal ischemia-reperfusion injury
    (Springer Wien, 2017) Basbug, Murat; Yildar, Murat; Yaman, Ismail; Cavdar, Faruk; Ozkan, Omer Faruk; Aksit, Hasan; Ozyigit, Musa Ozgur
    Background Acute mesenteric ischemia is a life-threatening clinical entity. 2-Aminoethoxydiphenyl borate (2-APB) is a membrane-permeable modulator of intracellular inositol triphosphate-induced calcium release. We investigated the effects of different 2-APB doses on intestinal ischemia-reperfusion injury in an experimental rat model. Methods We divided 24 Wistar albino rats into four groups: sham, control, ischemia-reperfusion +2 mg/kg 2-APB, and ischemia-reperfusion +4 mg/kg 2-APB. The sham group only underwent laparotomy for 1 h 30 min. A 30-min period of mesenteric ischemia was induced in the control and two treatment groups, followed by 1 h of reperfusion. Before the laparotomy, 2 mg/kg and 4 mg/kg 2-APB was administered i.v. in the treatments groups, and blood samples were collected after reperfusion. Serum levels of malondialdehyde, superoxide dismutase, glutathione, total antioxidant capacity, tumor necrosis factor (TNF)-alpha, and interleukin-6 were analyzed. Intestinal tissues were taken for histopathological, DNA fragmentation, and terminal deoxynucleotidyl transferase dUTP nick end labeling analyses to determine the proportion of apoptotic cells. Results 2-APB reduced serum malondialdehyde, TNF-alpha, and interleukin-6 levels. However, superoxide dismutase and total antioxidant capacity levels increased significantly in the 4-mg/kg 2-APB group (p < 0.05). The intestinal histopathological injury scores were significantly higher in the control group; these injuries were prevented in the 4-mg/kg 2-APB dose group. DNA damage after ischemia-perfusion decreased significantly in the 4-mg/kg 2-APB group compared with the control group. Conclusion 2-APB decreases oxidative stress and cell injury. Administering 4 mg/kg 2-APB prevented ischemia-perfusion injury by diminishing histological damage.
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    EFFECTS OF BORIC ACID IN AN EXPERIMENTAL RAT MODEL OF HEPATIC ISCHEMIA-REPERFUSION INJURY
    (Carbone Editore, 2015) Basbug, Murat; Yildar, Murat; Yaman, Ismail; Ozkan, Omer Faruk; Aksit, Hasan; Cavdar, Faruk; Sunay, Fatma Bahar
    Introduction: Hepatic ischemia-reperfusion injury can cause serious damages and affect distant organs. Boric acid is a antioxidant agent in ischemia/reperfusion injury. The aim of this study was to investigate the effects of boric acid in a rat model of hepatic ischemia-reperfusion injury. Material and methods: 30 rats were divided into three groups: sham, ischemia reperfusion and ischemia-reperfusion+boric acid. The sham group underwent only the surgical stress procedure. In the ischemia-reperfusion group, liver ischemia was induced by clamping the hepatic pedicle for 45 minute, followed by reperfusion for 1 hour. In the ischemia-reperfusion +boric acid group, the therapeutic agent boric acid was administered intraperitoneally, 10 minute before clamping the hepatic pedicle. Serum levels of malondialdehyde, superoxide dismutase, glutathione, total antioxidant capacity, tumor necrosis factor-alpha, interleukin-6, aspartate aminotransferase, alanine aminotransferase, Gamma-glutamyl transferase were determined. Liver tissues were taken for histopathological examination, DNA fragmentation, and TUNEL staining to determine the apoptotic index. Results: Boric acid moderately reduced serum levels of malondialdehyde, tumor necrosis factor-alpha, interleukin-6. aspartate aminotransferase, gamma-glutamyl transferase in the ischemia-reperfusion injury group. Superoxide dismutase and alanine aminotransferase levels were decreased significantly in the boric acid-administered group (P < 0.05). The histopathological injury scores and the rate of apoptosis were significantly higher in the ischemia-reperfusion group; these injuries were reduced by boric acid administration. Conclusion: Our results demonstrate that boric acid decreases lipid peroxidation and enhances the antioxidant defense mechanism. This study showed that boric acid might protect against ischemia-reperfusion injury in this rat model.