Browsing by Author "Akyol, O"

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Effects of Aminoguanidine and Antioxidant Erdosteine on Bleomycin-Induced Lung Fibrosis in Rats
(Academic Press inc Elsevier Science, 2004) Yildirim, Z; Turkoz, Y; Kotuk, M; Armutcu, F; Gurel, A; Iraz, M; Akyol, O
Reactive oxygen and nitrogen species have been implicated in the pathogenesis of bleomycin -induced lung fibrosis. The effects of aminoguanidine and erdosteine on the bleomycin-induced lung fibrosis were evaluated in rats. The animals were placed into five groups: Vehicle + vehicle, vehicle + bleomycin (2.5U/kg), bleomycin + aminoguanidine (200mg/kg), bleomycin + erdosteine (10mg/kg), and bleomycin + erdosteine + aminoguanidine. Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxyproline content and lung histology, which is completely prevented by erdosteine and aminoguanidine. A strong staining for nitro tyrosine antibody in lung tissue and increased levels of lung NO were found in bleomycin group, that were significantly reduced by aminoguanidine and erdosteine. Aminoguanidine and erdosteine significantly prevented depletion of superoxide dismutase and glutathione peroxidase and elevated myeloperoxidase activities, malondialdehyde level in lung tissue produced by bleomycin. Data presented here indicate that aminoguanidine and erdosteine prevented bleomycin-induced lung fibrosis and that nitric oxide mediated tyrosine nitration of proteins plays a significant role in the pathogenesis of bleomycin-induced lung fibrosis. Also our data suggest that antifibrotic affect of antioxidants may be due to their inhibitory effect on nitric oxide generation in this model. (C) 2004 Elsevier Inc. All rights reserved.
Erdosteine Ameliorates Neurological Outcome and Oxidative Stress Due To Ischemia/Reperfusion Injury in Rabbit Spinal Cord
(W B Saunders Co Ltd, 2004) Ege, E; Ilhan, A; Gurel, A; Akyol, O; Ozen, S
Objective. Oxygen-derived free radicals have been suggested as important in degeneration after spinal cord ischemia. The aim of this study was to investigate whether erdosteine has a protective effect against spinal cord ischemia during aortic cross clamping. Materials and methods. New Zealand White rabbits (n = 21) were divided into three groups. In the ischemia/reperfusion group (I/R) (n = 8), the infrarenal aorta of rabbits was cross clamped for 21 min and then reperfused. In erdosteine group, the administration of erdosteine solution (50 mg/kg) was started two days before aortic cross-clamping and rabbits (n = 8) were subjected to ischemia and reperfusion. Animals in control group (n = 5) underwent a surgical procedure similar to the other groups but the aorta was not clamped. The animals were sacrificed at 72 h and histopathological, and biochemical analyses were carried out on the lumbar spinal cords. Results. Erdosteine treatment zoos associated with improved neurological function in the postoperative period. Histopathological examination of spinal cord tissues in erdosteine group revealed changes consistent with mild ischemic injury, but rabbits in I/R group with paraplegia had total destruction of the motor neurons. Biochemical analyses of spinal cord tissues, in the I/R group, revealed a significant increase in the superoxide dismutase, xanthine oxidase, adenosine deaminase and myeloperoxidase activities, and a significant depletion in glutathione peroxidase activity when compared to that of control rabbits. Erdosteine treatment prevented the increase of all these enzymes except adenosine deaminase. Ischemia/reperfusion produced a significant increase in the tissue malondialdehyde levels. Ischemia/reperfusion-induced increments in malondialdehyde content of the spinal cord were significantly prevented by erdosteine treatment. Conclusions. The present study demonstrated that erdosteine treatment before aortic cross clamping ameliorates neurological outcome, neuronal injury and oxidative stress in the rabbit spinal cord.
Erdosteine Prevents Bleomycin-Induced Pulmonary Fibrosis in Rats
(Elsevier, 2004) Sogut, S; Ozyurt, H; Armutcu, F; Kart, L; Iraz, M; Akyol, O; Yildirim, Z
Oxidative stress plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. Therefore, erdosteine, an antioxidant, is expected to have an inhibitor potential against the disease. Rats were given one dose of bleomycin in pulmonary fibrosis groups and saline in controls. The first dose of oral erdosteine (10 mg/kg/day) was given 2 days before the bleomycin injection to achieve the plateau level in blood and continued until killing. At day 14, fibrotic changes were evaluated, using Aschoft's criteria and lung hydroxyproline content. Bleomycin produced a fivefold increase in fibrosis score that was decreased by 87% by erdosteine (P>0.001) and almost twofold increases in hydroxyproline content which were completely prevented by erdosteine. Myeloperoxidase activities and MDA levels, which were significantly higher in the bleomycin group, were then significantly attenuated by erdosteine. These results revealed that oral erdosteine may prevent the development of acute pulmonary inflammation caused by bleomycin injection via the repression of neutrophil accumulation and lipid peroxidation, resulting in the inhibition of subsequent lung fibrosis. (C) 2004 Elsevier B.V. All rights reserved.
Ginkgo Biloba Prevents Mobile Phone-Induced Oxidative Stress in Rat Brain
(Elsevier, 2004) Ilhan, A; Gurel, A; Armutcu, F; Kamisli, S; Iraz, M; Akyol, O; Ozen, S
Background: The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats. Methods: Rats (EMR+) were exposed to 900 MHz EMR from NIP for 7 days (1 h/day). In the EMR + Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups. Results: Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically. Conclusion: Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue. (C) 2003 Elsevier B.V. All rights reserved.