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    Critical time point for apoptotic cell death in an experimental ischemia/reperfusion model and the effect of N-acetylcystein [Deneysel iskemi/reperfüzyon modelinde apoptotik hücre ölümü için kritik zamanlama ve N-asetilsistein’in etkisi]
    (Turkish Biochemistry Society, 2017) Ozsarlak-Sozer G.; Emre M.; Demirkol S.; Açıkalın A.; Çetiner S.; Topçu Z.; Demir-Dora D.
    Objective: Kidney transplantation is an important treatment option in end stage renal failure. Tissue death may be an important problem when a kidney is removed from a cadaver and transported to a donor a long distance away. The purpose of this study is to determine the critical time point for apoptotic cell death in a renal ischemia/reperfusion model and determine the effects of N-acetylcystein on apoptosis induced by ischemia injury. Methods: Apoptotic cell death after induced renal ischemia followed by reperfusion, was estimated in a group of Wistar albino rats by immunoflourescence and ELISA techniques. N-acetylcystein, an antioxidant agent, was given to the rats to study the effect on apoptosis. Tissues were examined immunohistochemically at 0, 1 h, 24 h, 5 days and 10 days for detection of apoptotic cells. Results: Our results showed that an ischemia for 60 min followed by reperfusion for 60 min triggered apoptosis. Moreover, N-acetylcystein significantly diminished both the ischemia/reperfusion damage and apoptosis. Conclusion: We anticipate our results would be important for kidney transplantation in estimating the critical time point for apoptosis and administration of N-acetylcystein prior to removal of the organ may be important in delaying the onset of apoptosis. © 2017, Turkish Biochemistry Society. All rights reserved.
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    Glutathione depletion by buthionine sulfoximine induces oxidative damage to DNA in organs of rabbits in vivo
    (2009) Gokce G.; Ozsarlak-Sozer G.; Oktay G.; Kirkali G.; Jaruga P.; Dizdaroglu M.; Kerry Z.
    Glutathione (GSH) exists in mammalian tissues in vivo at high concentrations and plays an important protective role against oxidatively induced damage to biological molecules, including DNA. We investigated oxidatively induced damage to DNA by GSH depletion in different organs of rabbits in vivo. Rabbits were treated subcutaneously with buthionine sulfoximine (BSO), an effective GSH-depleting compound. GSH levels were measured in heart, brain, liver, and kidney of animals. BSO treatment significantly reduced GSH levels in heart, brain, and liver, but not in kidney. DNA was isolated from these tissues to test whether GSH depletion causes oxidatively induced DNA damage in vivo. Gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry with isotope dilution methods were applied to measure typical products of oxidatively induced damage in isolated DNA samples. Several such products were identified and quantified in all organs. BSO treatment caused significant formation of 8-hydroxyguanine, 2,6-diamino-4- hydroxy-5-formamidopyrimidine, 8-hydroxyadenine, and (5'S)-8,5'- cyclo-2'-deoxyadenosine in DNA of organs of rabbits. Animals were fed with the semiessential amino acid 2-aminoethanesulfonic acid (taurine) during BSO treatment. Taurine significantly inhibited GSH depletion and also formation of DNA products. Depletion of GSH correlated well with formation of DNA products, indicating the role of GSH in preventing oxidatively induced DNA damage. Our findings might contribute to the understanding of pathologies associated with DNA damage, oxidative stress, and/or defective antioxidant responses and improve our understanding of the effect of BSO in increasing the efficacy of anticancer therapeutics. © 2009 American Chemical Society.
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    Low-dose fluvastatin prevents the functional alterations of endothelium induced by short-term cholesterol feeding in rabbit carotid artery
    (2012) Sevin G.; Akcay Y.D.; Ozsarlak-Sozer G.; Yasa M.
    3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, commonly known as statins, are the medical treatment of choice for hypercholesterolemia. In addition to lowering serum-cholesterol levels, statins appear to promote pleiotropic effects that are independent of changes in serum cholesterol. In this study, we investigated the effects of low-dose fluvastatin on antioxidant enzyme activities (superoxide dismutase, SOD; catalase), total nitrite/nitrate levels, and vascular reactivity in 2% cholesterol-fed rabbits. This diet did not generate any fatty streak lesions on carotid artery wall. However, SOD activity significantly increased with cholesterol feeding whereas the catalase activities decreased. The levels of nitrite/nitrate, stable products of NO degradation, diminished. Moreover, dietary cholesterol reduced vascular responses to acetylcholine, but contractions to serotonin were augmented. Fluvastatin treatment abrogated the cholesterol-induced increase in SOD, increased the levels of nitric oxide metabolites in tissue, and restored both the impaired vascular responses to acetylcholine and the augmented contractile responses to serotonin without affecting plasma-cholesterol levels. Phenylephrine contractions and nitroglycerine vasodilatations did not change in all groups. This study indicated that fluvastatin treatment performed early enough to improve impaired vascular responses may delay cardiovascular complications associated with several cardiovascular diseases. Copyright 2012 Gulnur Sevin et al.