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Alacam H.,Ondokuz Mayis University | Avci B.,Ondokuz Mayis University | Salis O.,Mental Health and Diseases Hospital | Dilek A.,Ondokuz Mayis University | And 4 more authors.
Turkish Journal of Medical Sciences | Year: 2013

Aim: Asymmetric dimethylarginine (ADMA) is an inhibitor of nitric oxide synthase (NOS). Oxidative stress might be defined as an imbalance between protein oxidation and antioxidants. Our aim was to determine in vivo whether ADMA causes oxidative damage. Materials and methods: Thirty rats were divided into 3 equal groups: a control group, a group administered 1 mg/kg ADMA, and a group administered 2 mg/kg ADMA. ADMA was administered intraperitoneally for 7 days. Malondialdehyde (MDA), protein carbonyl (PC) content, and nitrate+nitrite concentrations were measured with serum samples. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) activities were analyzed with plasma samples. Results: A significant increase in MDA concentration was observed in the ADMA groups, but this increase was not dose-dependent. However, no significant changes in PC content or nitrate+nitrite concentration were observed. Furthermore, catalase, SOD, and GSHPx activity was suppressed in the ADMA groups. Suppression of GSH-Px activity was dose-dependent. Conclusion: ADMA results in oxidative damage in vivo with lower doses than in NOS inhibition. ADMA has more of an oxidative effect on lipids than it does on proteins. Antioxidant enzymes must be consumed in significant amounts to remove the stress produced by ADMA. © Tübi̇tak. Source


Duzgun A.,Ankara Branch of Council of Forensic Medicine | Bedir A.,Ondokuz Mayis University | Ozdemir T.,Gazi State Hospital | Nar R.,Aksaray State Hospital | And 4 more authors.
Indian Journal of Biochemistry and Biophysics | Year: 2013

The endoplasmic reticulum (ER) is related to the various signal routes that are activated in unfolded protein response (UPR). The Grp78, Grp94, CHOP, MTJ1 and HMOX1 genes expressions demonstrate UPR activity. In this study, we investigated the UPR gene expressions in larynx epidermoid carcinoma (HEp2) to which dexamethasone (dex) was applied. HEp2 cells were administered for 48 h with different combinations using 0.1 μM and 1 μM dex, 1 mM phenyl butyric acid (PBA) and 100 ng/ml lipopolysaccharide (LPS). The Grp78, Grp94, CHOP, MTJ1 and HMOX1 genes expression was determined using quantitative RT-PCR. The Grp78, MTJ1 and HMOX1 gene expression increased with the administration of 1 μM dex. CHOP expression, on the other hand, decreased with 0.1 μM dex. When dex was combined with LPS, nearly all gene expressions decreased. The increase in Grp78, Grp94, HMOX1 and MTJ1 gene expression was greater in groups in which dex was administered in combination with PBA than in groups in which dex was administered alone. Dex in low dose (0.1 μM) caused a decrease in CHOP expression in HEp2 cells and an increase in Grp78 expression, in particular. The changes in UPR genes expressions may lead to the extended survival of the cells. Source


Alacam H.,Ondokuz Mayis University | Karli R.,Ondokuz Mayis University | Alici A.O.,Samsun Education and Research Hospital | Avci B.,Ondokuz Mayis University | And 6 more authors.
Human and Experimental Toxicology | Year: 2013

Our aim in this study is to examine the effects of α-tocopherol (AT) on rats with aspiration pneumonitis induced with bile acids (BAs). The animals were divided in to four groups, namely saline group (n = 7), saline + AT group (n = 7), BA group (n = 7), and BA + AT group (n = 7). Saline and BA groups aspirated intratracheally with 1 ml/kg saline and 1 ml/kg bile acids, respectively. AT was given at 20 mg/kg/day dosage for 7 days to the groups. AT group was given 20 mg/kg/day AT for 7 days. Malondialdehyde (MDA), Clara cell protein 16 (CC-16), catalase (CAT), superoxide dismutase (SOD), as well as peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar edema, alveolar exudate, alveolar histiocytes, and necrosis were evaluated. The CAT activity of the BA group was significantly lower than the saline group. In the BA + AT group, there was a significant increase in SOD and CAT activities when compared with that of the BA group. The CC-16 and MDA contents in the BA group were significantly higher than in the saline group. The CC-16 and MDA levels of the BA + AT group were significantly lower than BA group. Histopathologic changes were seen in BA group, and there was a significant decrease in the BA + AT group. In conclusion, AT might be beneficial in the treatment of aspiration pneumonitis induced by BAs because AT decreased oxidative damage and resulted in a decrease in CC-16 levels. © The Author(s) 2013. Source


Nar R.,Aksaray State Hospital | Bedir A.,Ondokuz Mayis University | Alacam H.,Ondokuz Mayis University | Kilinc V.,Ondokuz Mayis University | And 3 more authors.
Tumor Biology | Year: 2012

Our purpose in this study is to analyze mitochondrial DNA (mtDNA) lesion frequencies and mtDNA 4977 deletion in HepG2 cells to examine the effects of ouabain on mtDNA. HepG2 cells were treated with 0.75, 7.5, 75, and 750 nM of ouabain for 24 h in the presence and absence of 10 mM 2-deoxyglucose (2-DG). The frequency of mtDNA 4977 deletions and mitochondrial lesions were determined by real-time polymerase chain reaction. A ≥1.2-fold change or greater was considered significant. Ouabain doses of 750, 75, and 7.5 nM alone increased the frequency of mtDNA 4977 deletions 1.39, 1.92, and 1.44 times, respectively. The 750 and 75 nM ouabain doses combined with 2-DG increased the mtDNA 4977 deletion frequency 4.94 and 1.57 times, respectively. The 750 and 75 nM ouabain doses alone increased the mtDNA lesion frequency 2.5 and 1.5 times, respectively. The 750 nM ouabain dose combined with 2-DG increased the mtDNA lesion frequency 2.28 times. The 7.5 nM ouabain dose alone and combined with 2-DG decreased the mtDNA lesion frequency 0.67 and 0.45 times, respectively. Ouabain alone and when combined with 2-DG increases mtDNA lesion and mtDNA 4977 deletion frequencies. This supports the thesis that ouabain creates oxidative stress and induces DNA damage and apoptosis. © 2012 International Society of Oncology and BioMarkers (ISOBM). Source

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