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    Brief communication: Omega-3 essential fatty acid supplementation and erythrocyte oxidant/antioxidant status in rats
    (2005) Iraz M.; Erdogan H.; Ozyurt B.; Ozugurlu F.; Ozgocmen S.; Fadillioglu E.
    Fish oil contains large amounts of essential omega-3 fatty acids, such as eicosapentaenoic and docosahexaneoic acids, which are building structures of cell membranes. The goal of this study was to elucidate the effects of dietary omega-3 fatty acid supplementation on the oxidant/antioxidant status of erythrocytes in rats. The malondialdehyde (MDA) and nitric oxide (NO) levels and the catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) activities were assayed in erythrocytes of male Wistar albino rats after 30 days of dietary supplementation with fish oil (0.4 g/kg/day). Erythrocyte CAT activity in the treated group was increased in comparison with the control group. Erythrocyte MDA and NO levels were lower in the treated group than the controls. Erythrocyte GSH-Px and SOD activities did not differ significantly in the 2 groups. Negative correlations were found between SOD and CAT activities, and between SOD and GSH-Px activities in the treated group. In conclusion, omega-3 fatty acid supplementation helps to prevent lipid peroxidation and to safeguard erythrocytes from oxidative injury. Dietary supplementation with omega-3 fatty acids might possibly protect tissues from oxygen free radical injury in the various diseases in which the oxidant/antioxidant defense mechanisms are disturbed. © 2005 by the Association of Clinical Scientists, Inc.
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    Effect of BQ-123 and nitric oxide inhibition on liver in rats after renal ischemia-reperefusion injury
    (2006) Emre M.H.; Erdogan H.; Fadillioglu E.
    Ischemia-reperfusion (I/R) injury induces an inflammatory response and production of oxygen-derived reactive species which affect many organs including heart, brain, kidney and gastrointestinal tract. The aim of this study was to assess the hepatic changes after renal I/R injury. Male Sprague Dawley rats were subjected to either sham operation or treatment with L-NAME, L-arginine and BQ-123 during 30 min renal ischemia and 2 h reperfusion injury. Hepatic superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) activities, and thiobarbituric acid-reactive substances (TBARS) and nitric oxide (NO) levels were evaluated to show hepatic response to renal I/R injury. Catalase and SOD activities showed significant differences between the control and the other groups after I/R. On the other hand, GSH-Px activity did not show any significant changes between the control and the other experimental groups mentioned under above conditions. Meanwhile, levels of TBARS were not different between the control and the other experimental groups, whereas NO level showed changes between the control and experimental groups except the one to which endothelin receptor antagonist agent (BQ-123) subjected. Experimental period may not be enough to determine the changes in GSH-Px activity and level of TBARS. However, catalase and SOD activities decreased in experimental groups treated by chemical agents. NO level decreased in chemicalagent-applied experimental groups but not in the group to which endothelin receptor antagonist BQ-123 was applied alone.
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    Melatonin improves methanol intoxication-induced oxidative liver injury in rats
    (Blackwell Publishing Ltd, 2007) Kurcer Z.; O?uz E.; Iraz M.; Fadillioglu E.; Baba F.; Koksal M.; Olmez E.
    This study was performed to evaluate the effect of melatonin on methanol-induced liver injury. We evaluated the levels of malondialdehyde (MDA), protein carbonylation (PC), myeloperoxidase (MPO) activities and to assess lipid peroxidation, protein oxidation, neutrophil accumulation and nitrite which is a stable end product of nitric oxide respectively. We also studied superoxide dismutase, catalase, and glutathione peroxidase activities of liver tissue to evaluate the changes in the antioxidant status. Histopathological alterations were also determined. The experiment was performed on Wistar rats, which received intragastric 3 g/kg methanol as a 50% solution in isotonic saline once. After 6 and 24 hr all the drug received and intoxicated rats were killed under anesthesia. Pretreatment with melatonin (10 mg/kg) decreased the MDA levels significantly, restored the PC levels to the control, prevented the increase of nitrite level and MPO activity significantly and reversed to the control levels, prevented the reduction in all of the antioxidant enzyme activities. Additionally in melatonin treated group piecemeal necrosis, lobular lytic necrosis, and portal inflammation returned to normal histologic appearances when compared with methanol administration. In conclusion, melatonin has protective effects against methanol-induced hepatic injury. © 2007 The Authors.