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Öğe Effects of erdosteine on cyclosporin-A-induced nephrotoxicity(Sage Publications Ltd, 2012) Tutanc, M.; Arica, V.; Yilmaz, N.; Nacar, A.; Zararsiz, I.; Basarslan, F.; Tutanc, O. D.Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group I rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.Öğe Effects of erdosteine on hemostasis: An experimental study(Sage Publications Ltd, 2012) Tutanc, M.; Arica, V.; Motor, S.; Basarslan, F.; Erden, E. S.; Ozturk, O. H.; Zararsiz, I.Aim: In this study, the effects of erdosteine (ED) on the platelet function and coagulation were investigated in adult rats. Materials and Method: Twenty-eight male Wistar albino rats were divided into four groups. The control rats in group I (n = 7) were given only 0.5 cc of normal saline daily through oral gavage. Group II (n = 7) rats were administered 3 mg/kg ED through oral gavage for 3 days; while group III (n = 7) rats were given 10 mg/kg ED through oral gavage for 3 days; and group IV (n = 7) rats were administered 30 mg/kg ED through oral gavage for 3 days. Prothrombin time (PT), activated prothromboplastin time (aPTT), international normalized ratio (INR), coagulation factors and complete blood counts were measured from the blood drawn. Results: There were a lot of differences between ED groups and control group, and among ED groups. The found differences were level of PT, aPTT, INR, coagulation factors, and number of platelets. Discussion: We consider that ED which is used as a mucolytic agent in child clinics may affect hemostasis and coagulation in a dose-dependent manner. ED should be used carefully by the patients with coagulation disorders, since there is no information available in the package insert and literature screening regarding the effect of ED.Öğe Isolated brainstem edema in a pediatric patient with head trauma: a case report(Verduci Publisher, 2015) Basarslan, K.; Basarslan, F.; Karakus, A.; Yilmaz, C.Brain stem is the most vital part of our body and is a transitional region of the brain that connects the cerebrum with the spinal cord. Though, being small in size, it is full of indispensible functions such as the breathing, heart beat. Injury to the brain stem has similar effects as a brain injury, but it is more fatal. Use of the Glasgow Coma Score as a prognostic indicator of outcome in patients with head injuries is widely accepted in clinical practice. Traumatic brain stem edema in children is rare, but is associated with poor outcome. The question is that whether it is being aware of computerized tomography appearance of the posterior fossa when initial evaluating pediatric patients with head trauma at emergency clinics. Normal and edematous brain stem without an additional pathology are slightly different and not distinguished easily. On the other hand, brain stem edema should be promptly identified and appropriately treated in a short time.Öğe N-Acetylcysteine prevents doxorubucine-induced cardiotoxicity in rats(Sage Publications Ltd, 2013) Arica, V.; Demir, I. H.; Tutanc, M.; Basarslan, F.; Arica, S.; Karcioglu, M.; Ozturk, H.This study is designed to observe the effects of N-acetylcysteine (NAC) on doxorubucine-induced cardiac toxicity in rats both histologically and biochemically. Totally 32 rats divided equally into four groups were studied. The first group received only 200 mg/kg NAC intraperitoneal (i.p.) once every 24 h for 5 days (group 1); the second group received 20 mg/kg doxorubucine (DOX) i.p. single dose plus NAC 200 mg/kg i.p. once every 24 h for 5 days (group 2); the third group received DOX 20 mg/kg DOX i.p. single dose (group 3) and the fourth group, which is also the control group, received saline (group 4). Following 24 h of the final dose, blood samples were drawn from a portal vein and heart tissue were obtained. Tissue thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) levels were highest in the DOX group. In the DOX-treated rats, serum TBARS, NO, aspartate transaminase, lactate dehydrogenase and creatine kinase levels were highest when compared with other groups. Except for serum superoxide dismutase levels, all other parameters differed significantly between the DOX plus NAC group and the DOX group. In the DOX plus NAC group, general architecture was preserved better than the DOX group and myofibril loss was minimal compared with the DOX group. NAC demonstrated, both biochemically and histologically, to be effective in the prevention of DOX-induced cardiotoxicity in rat models. Evaluation of NAC's effect on DOX toxicity warrants further clinical trials on cancer patients.Öğe Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats(Sage Publications Ltd, 2012) Basarslan, F.; Yilmaz, N.; Ates, S.; Ozgur, T.; Tutanc, M.; Motor, V. K.; Arica, V.Aim: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. Materials and methods: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. Results: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. Conclusion: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.
