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    Amelioration of subchronic acrylamide toxicity in large intestine of rats by organic dried apricot intake
    (Tubıtak scıentıfıc & technıcal research councıl turkey, ataturk bulvarı no 221, kavaklıdere, ankara, 00000, turkey, 2015) Erdemli, Mehmet Erman; Dogan, Zumrut; Cigremis, Yilmaz; Akgoz, Muslum; Altintoz, Eyup; Gecer, Murat; Turkoz, Yusuf
    Acrylamide (AA) has neurotoxic, mutagenic, and genotoxic effects in humans and experimental animals. Fruit consumption is important for human health, because fruits are the source of many nutrients such as vitamins, minerals, carotenoids, dietary fiber, and phytonutrients. Many agricultural products provide natural melatonin in the diet. At the onset of the study, rats were weighted and randomly divided into four groups each containing 10 rats as follows: group 1: control (fed with normal diet and normal drinking water); group 2: apricot (fed with a daily diet with 5% apricot and normal drinking water); group 3: AA (administered daily acrylamide at 500 mu g/kg b.w. via drinking water and fed a normal diet); group 4: apricot-AA (administered daily acrylamide at 500 mu g/kg b.w. via drinking water and fed with a diet with 5% apricot). The diet schedule was continued for 12 weeks. At the end of the study, samples of large intestine were collected for biochemical analyses. The highest lipid peroxidation (as malondialdehyde, MDA) levels were observed in the AA groups, but MDA levels decreased significantly (P < 0.05) with apricot intake. Glutathione peroxidase activity in the apricot-AA group was higher than in the other three groups (P < 0.05). Glutathione S-transferase (GST) enzyme activity increased significantly in the AA group as compared with the other groups (P < 0.05). However, GST activity was significantly (P < 0.05) decreased by the apricot-supplemented diet. GST-Pi mRNA levels in the AA group increased significantly (P < 0.05) as compared with the other groups. In conclusion, the results of the current study demonstrated that AA caused large intestine damage and showed the efficiency of apricot in preventing this damage by inhibiting lipid peroxidation and improving antioxidant enzyme activities.
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    Resveratrol ameliorates cisplatin-induced oxidative injury in New Zealand rabbits
    (Canadian Science Publishing, 2015) Cigremis, Yilmaz; Akgoz, Muslum; Ozen, Hasan; Karaman, Musa; Kart, Asim; Gecer, Murat; Atalan, Gultekin
    This study investigated the preventive role of resveratrol in cisplatin-induced nephrotoxicity. The study used groups of New Zealand rabbits that were treated as follows: group C (cisplatin treated), group R (resveratrol treated), group R+C (resveratrol + cisplatin treatment), and group E (control group). Kidney levels of glutathione were significantly lower in group C than in groups E and R, whereas glutathione levels in group R+C were found to be similar to the control values. Malondialdehyde levels in group C were significantly higher than in groups E and R. However, malondialdehyde levels in group R+C were similar to group E. Kidney levels of nitric oxide were significantly higher in the cisplatin group than in the control, whereas nitric oxide levels were at basal values in group R+C. Cisplatin treatment significantly reduced kidney levels of glutathione peroxidase, superoxide dismutase, and catalase activity compared with those of group E, whereas resveratrol treatment significantly increased levels of glutathione peroxidase, superoxide dismutase, and catalase activity in group R+C. However, cisplatin injection did not affect mRNA levels of glutathione peroxidase, superoxide dismutase, or catalase enzymes. Histopathological and immunohistochemical analyses indicated that cisplatin caused kidney damage, which was mostly prevented by resveratrol treatment. In conclusion, resveratrol ameliorates cisplatin-induced oxidative injury in the kidney of rabbit.