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    Protective Effect of ?-Carotene on Methotrexate-Induced Oxidative Liver Damage
    (Sage Publications Inc, 2010) Vardi, Nigar; Parlakpinar, Hakan; Cetin, Asli; Erdogan, Ali; Ozturk, I. Cetin
    In this study, the authors aimed to investigate the role of oxidative stress on the hepatic damage caused by methotrexate (MTX) and the possible protective effects of beta-carotene against this damage. The rats were divided into four groups as control, MTX (20 mg/kg ip), beta-carotene (10 mg/kg/day ip) | MTX, and beta-carotene. Histopathologic alterations were evaluated for defining the liver damage. The tissue, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GP-x) contents and serum aspartate aminotransferase (AST) and alanine aminotranferase (ALT) activities were also examined. Histopathologic damage for each group score findings have been determined as control: 0.66 +/- 0.33; MTX: 7.0 +/- 0.68; beta-carotene | MTX: 3.3 +/- 0.42; and beta-carotene: 0.5 +/- 0.3. In the MTX-treated group, MDA, AST, and ALT values were increased, while SOD and GP-x values were decreased compared with the control group. In the beta-carotene + MTX-treated group, AST and ALT values significantly decreased, while all other parameters were similar to the control group. This study shows that beta-carotene has a protective effect on MTX-induced oxidative hepatic damage. Consequently, it seems that an antioxidant agents like beta-carotene may be useful in decreasing the side effects of chemotherapy.
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    Protective effect of apricot (Prunus armeniaca L.) on hepatic steatosis and damage induced by carbon tetrachloride in Wistar rats
    (Cambridge Univ Press, 2009) Ozturk, Feral; Gul, Mehmet; Ates, Burhan; Ozturk, I. Cetin; Cetin, Asli; Vardi, Nigar; Otlu, Ali
    The present study was planned to investigate the protective effect of 10% and 20% apricot-containing feed on carbon tetrachloride (CCl4)-induced hepatic steatosis and damage. Adult male Wistar rats (it 42) were divided into six groups of seven each, as follows: control group; CCl4 group; CCl4 + 10% apricot group; CCl4 + 20% apricot group; 10% apricot group; 20% apricot group. All apricot groups were fed with 10% or 20% apricot-containing feed for 5 months. CCl4 injections were applied to the CCl4 groups at the dose of 1 mg/kg for 3 d at the end of 5 months. In the CCl4 group, vacuolated hepatocytes and hepatic necrosis were seen, especially in the centrilobular area. Hepatocytes showed an oedematous cytoplasmic matrix, large lipid globules and degenerated organelles. The area of liver injury was found significantly decreased with apricot feeding. Malondialdehyde and total glutathione levels and catalase, superoxide dismutase and glutathione peroxidase activities were significantly changed in the CCl4 group and indicated increased oxidative stress. Apricot feeding decreased this oxidative stress and ameliorated histological damage. We concluded that apricot feeding had beneficial effects on CCl4-induced liver steatosis and damage probably due to its antioxidant nutrient (beta-carotene and vitamin) contents and high radical-scavenging capacity. Dietary intake of apricot can reduce the risk of liver steatosis and damage caused by free radicals.