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    Changes in nitric oxide levels and antioxidant enzyme activities may have a role in the pathophysiological mechanisms involved in autism
    (Elsevier Science Bv, 2003) Sögüt, S; Zoroglu, SS; Özyurt, H; Yilmaz, HR; Özugurlu, F; Sivasli, E; Yetkin, Ö
    Background: There is evidence that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. Although it has not been investigated yet, several recent studies proposed that nitric oxide (NO) and other parameters related to oxidative stress may have a pathophysiological role in autism. Methods: We assessed the changes in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and thiobarbituric acid-reactive substances (TBARS) levels in plasma as well as NO levels in red blood cells (RBC) in patients with autism (n = 27) compared to age- and sex-matched normal controls (n = 30). Results: In the autistic group, increased RBC NO levels (p < 0.0001) and plasma GSH-Px activity (p < 0.0001) and unchanged plasma TBARS levels and SOD activity were detected. Conclusions: These findings indicate a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism. (C) 2003 Published by Elsevier Science B.V.
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    Comparison of serum nitric oxide, malondialdehyde levels, and antioxidant enzyme activities in Behcet's disease with and without ocular disease
    (Karger, 2004) Aydin, E; Sögüt , S; Özyurt, H; Özugurlu, F; Akyol, Ö
    Objective: The pathogenesis of Behcet's disease ( BD) may be related to excessive production of reactive oxygen species, activated neutrophils, and T lymphocytes. The goal of this prospective study was to investigate whether there is any relationship among the oxidant/ antioxidant system and nitric oxide ( NO) and malondialdehyde (MDA) levels in patients with BD and its subtypes: complete Behcet's disease (CBD) and incomplete Behcet's disease (ICBD), with or without ocular disease. Methods: Thirty-two patients and 26 age- and sex-matched healthy control subjects were evaluated for NO and MDA levels and antioxidant enzyme activities. The patients with BD were divided into two subgroups: those with and without ocular disease. Twelve patients with CBD and 4 patients with ICBD had ocular disease. The serum NO level was determined by Griess reaction. The MDA level was detected by thiobarbituric acid reaction. Superoxide dismutase ( SOD) and glutathione peroxidase (GSH-Px) activities in serum were analyzed with spectrophotometric methods. Results: Increased MDA levels but decreased GSH-Px activities in plasma were observed in BD patients with all subtypes, as compared with controls. Concerning the presence of ocular disease and the subtype ( CBD or ICBD) compared with each other, there were no significant differences in MDA or NO serum levels and SOD or GSH-Px enzyme activities. Conclusions: Serum NO levels and SOD enzyme activities were not significantly changed in patients with BD and its subtypes; however, a remarkable decrease of GSH-Px enzyme activity and increase of MDA levels were found. Copyright (C) 2004 S. Karger AG, Basel.
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    Degradation of vincristine by myeloperoxidase and hypochlorous acid in children with acute lymphoblastic leukemia
    (Pergamon-Elsevier Science Ltd, 2003) Özgen, O; Türköz, Y; Stout, M; Özugurlu, F; Pelik, F; Bulut, Y; Aslan, M
    Vincristine (VCR) is an effective drug against acute lymphoblastic leukemia (ALL), many solid tumors, but not acute myeloid leukemia. It has been hypothesized that resistance of myeloblasts to VCR is related to myeloperoxidase (MPO) and production of hypochlorous acid (HOCl). We investigated the relationship between VCR degradation and MPO expression and serum HOCl concentrations in pediatric patients with ALL, lymphoma and solid tumors. We studied the sera from 43 children, of which 23 were newly diagnosed and as yet untreated cancer patients, 10 on chemotherapy and 10 healthy control subjects. Patients' sera were incubated with VCR alone or in the presence of taurine (T) or acetaminophen (APAP) and post-incubation VCR and HOCL concentrations were measured. Significant correlations between serum MPO expression, HOCl concentrations and VCR degradation were seen. In the chemotherapy group, MPO-positive patients produced high levels of HOCl and reciprocally low post-incubation VCR levels. HOCl and VCR concentrations in this group were significantly different than other groups studied. Both APAP and T inhibited VCR degradation in the sera of the chemotherapy group but not to the same degree. The effects seen here were consistent for both ALL and the lymphoma/solid tumor cases. Our results indicate that HOCl can increase VCR degradation in vitro in the serum and this effect is significantly more pronounced in pediatric patients undergoing chemotherapy. (C) 2003 Elsevier Science Ltd. All rights reserved.
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    Role of caffeic acid phenethyl ester, an active component of propolis, against cisplatin-induced nephrotoxicity in rats
    (Wiley, 2004) Özen, S; Akyol, Ö; Iraz, M; Sögüt, S; Özugurlu, F; Özyurt, H; Odaci, E
    We have investigated the effect of caffeic acid phenethyl ester (CAPE) on cisplatin-induced nephrotoxicity in rats. Administration of a single dose of cisplatin resulted in the elevation of blood area nitrogen and creatinine in serum, as well as nitric oxide in kidney tissue of rats. Cisplatin also caused reduction of catalase (P < 0.0001), superoxide dismutase (P = 0.149) and glutathrone peroxidase (P < 0.0001) activities in kidney tissue. Although cisplatin caused elevation in malondialdehyde levels and myeloperoxidase activities in kidney tissue, they were not statistically significant. Caffeic acid phenethyl ester was found to be protective against cisplatin-induced antioxidant enzyme reductions. Treatment with free-radical scavenger CAPE attenuated the increase in plasma blood area nitrogen and kidney nitric oxide levels, and showed histopathological protection against cisplatin-induced acute renal failure. Extensive epithelial cell vacuolization, swelling, desquamation and necrosis were observed in the kidney of the cisplatin-treated rat. There were also larger tubular lumens in cisplatin-treated rats than those of the control and the CAPE groups. Caffeic acid phenethyl ester caused a marked reduction in the extent of tubular damage. It is concluded that administration of cisplatin imposes an oxidative stress to renal tissue and CAPE confers protection against the oxidative damage associated with cisplatin. This mechanism may be attributed to its free-oxygen-radical scavenging activity. Copyright (C) 2004 John Wiley Sons, Ltd.