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Öğe Beneficial effect of erdosteine on methotrexate-induced testicular toxicity in mice(Sage Publications Inc, 2010) Oktar, Sueleyman; Gokce, Ahmet; Aydin, Mehmet; Davarci, Muersel; Meydan, Sedat; Ozturk, Oktay Hasan; Koc, AhmetMethotrexate is used to treat certain types of cancer of the breast, skin, head and neck, or lung. Methotrexate can cause serious or life-threatening side effects on liver, lungs, kidneys, and immune system. Methotrexate chemotherapy causes testicular damage in humans. The aim of this study was to investigate the possible protective role of erdosteine on testicular toxicity of methotrexate in mice. Twenty-six male mice were divided into four groups as follows: group 1, control; group 2, erdosteine-treated; group 3, methotrexate-treated; and group 4, methotrexate + erdosteine treated. On the first day of experiment, a single dose of methotrexate was intraperitoneally administered to groups 3 and 4, although a daily single dose of erdosteine was orally administered to group 2 and 4 for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. The levels of total antioxidant capacity and total oxidative stress, and myeloperoxidase activity in the methotrexate group were higher than the control group (p<0.05). Lipid peroxidation levels were not changed in methotrexate group compared with control group. In conclusion, erdosteine could effectively protect the testes in methotrexate-induced toxicity.Öğe Erdosteine has dual effects on haemostasis via its different metabolites in young rats(Taylor & Francis Inc, 2010) Oktar, Sueleyman; Arica, Vefik; Tutanc, Murat; Ozturk, Oktay Hasan[Abstract Not Available]Öğe Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid(Elsevier Science Bv, 2009) Peker, Erdal; Oktar, Sueleyman; An, Mustafa; Kozan, Ramazan; Dogan, Murat; Cagan, Eren; Soeguet, SadikIn the present study, we investigated the effects of valproic acid (VPA) on nitric oxide (NO) level, lipid peroxidation, and antioxidant enzyme activities in 21 epileptic children and 26 healthy controls. The subjects were selected from those who visited for a checkup or medical treatment at the Mustafa Kemal University Research Hospital. Serum levels of NO-2, NO-3, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were analyzed by redox or enzymatic reactions and spectrophotometry. Based on the NO-2 and NO-3 levels, the NO concentration was about 10% higher in VPA group than in the control group (p < 0.001). However, no significant difference was detected for serum MDA, SOD, and CAT levels. It is suggested that NO would play a role in the mechanism of antiepileptic effects by VPA treatment. (c) 2009 Elsevier B.V. All rights reserved.Öğe Protective effects of tadalafil on experimental spinal cord injury in rats(Elsevier Sci Ltd, 2010) Serarslan, Yurdal; Yonden, Zafer; Ozgiray, Erkin; Oktar, Sueleyman; Guven, Esref Oguz; Sogut, Sadik; Yilmaz, NebiTadalafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Nitric oxide (NO) functions as a retrograde neurotransmitter in the spinal cord, and postsynaptic structures respond to NO by producing cGMP. The concentrations of cGMP in the spinal cord are controlled by the actions of PDE. The aim of the study was to evaluate and compare the effects of the use of both methylprednisolone and tadalafil on serum and tissue concentrations of NO, malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and tissue glutathione peroxidase (GSH-Px) activity in rats with spinal cord injury (SCI). SCI was induced in Wistar albino rats by dropping a 10 g rod from a 5.0 cm height at T8-10. The 28 rats were randomly divided into four equal groups: tadalafil, methylprednisolone, non-treatment and sham groups. Rats were neurologically tested at 24 hours after trauma. At the end of the experiment, blood samples were collected and spinal cord tissue samples were harvested for biochemical evaluation. The tissue level of NO was increased in the tadalafil group compared with the non-treatment and methylprednisolone groups (p < 0.05). The tissue levels of SOD and GSH-Px did not differ between the groups. Serum levels of NO were higher in the tadalafil group than in the non-treatment group (p < 0.05). The increase in serum SOD levels was greater in the tadalafil group than the methylprednisolone group. Serum MDA levels in the tadalafll and methylprednisolone groups tended to be lower than in the non-treatment group (p > 0.05). Tissue MDA levels in the taclalafil and methylprednisolone groups tended to be lower than in the non-treatment group and sham groups (p > 0.05). Although there was no difference in neurological outcome scores between the taclalafil, methylprednisolone and non-treatment groups (p > 0.05), the animals in the taclalafil and methylprednisolone groups tended to have better Scores than the non-treatment group. Thus, tadalafil appears to be beneficial in reducing the effects of injury to the spinal cord by increasing tissue levels of NO and serum activity of SOD. (C) 2009 Elsevier Ltd. All rights reserved.
