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Öğe Abdominal Ischemia-Reperfusion Induced Cardiac Dysfunction Can Be Prevented by MitoTEMPO(Taylor & Francis Inc, 2022) Akkoca, Ahmet; Celen, Murat Cenk; Tuncer, Seckin; Dalkilic, NizamettinBackground Cardiac dysfunction is secondary to acute mesenteric ischemia (AMI) and abdominal aortic aneurysms (AAA). The underlying cause of distant organ damage in the heart is the formation of oxidative stress caused by ischemia-reperfusion. In this study, we investigated the possible protective effects of a novel mitochondria-targeted antioxidant MitoTEMPO on contractile dysfunction and structural defects of the rat papillary muscle caused by abdominal ischemia-reperfusion (AIR). Methods and Results In the experiments, adult Wistar-Albino rats were used and animals were divided randomly into 3 groups; sham-operated group (SHAM), an IR group that had aortic cross-clamping for 1 h followed by 2 h reperfusion, and a third group that received protective 0.7 mg/kg/day MitoTEMPO injection for 28-day before IR. As a result, it was observed that MitoTEMPO injection had a protective effect on the mechanical activities and structural properties of the papillary muscle impaired by AIR. Our study also showed that AIR disrupted the contractile function of the papillary muscle for each stimulation frequency and post-potentiation responses tested. This is common for each measured and calculated mechanical parameter and MitoTEMPO injection showed its protective effects. Conclusion Consequently, calcium homeostasis seems to be impaired by AIR, and MitoTEMPO may exert its protective effect through energy metabolism by directly targeting the mitochondria.Öğe Can MitoTEMPO protect rat sciatic nerve against ischemia-reperfusion injury?(Springer, 2021) Tuncer, Seckin; Akkoca, Ahmet; Celen, Murat Cenk; Dalkilic, NizamettinAbdominal ischemia-reperfusion (I/R) is known to cause both structural and functional damage to sciatic nerve which is related to the oxidative stress. We investigated the protective effects of mitochondria-targeted antioxidant (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride (MitoTEMPO) on ischemia-reperfusion-induced nerve damage by using the conduction velocity distribution (CVD) calculations from in vitro compound nerve action potential (CNAP) recordings from rat sciatic nerve. Adult male Wistar albino rats were divided into three groups. The IR and IR + MT groups had aortic cross-clamping for 1 h followed by 2 h reperfusion, while SHAM group had the same procedure without cross-clamping. IR + MT group received 0.7 mg/kg/day MitoTEMPO injection for 28 days before I/R, while other groups received vehicle alone. Ischemia-reperfusion resulted in a significant decrease (p < .05) in maximum depolarizations (mV), areas (mV.ms), and maximum and minimum upstroke velocities (mV/ms) of CNAPs, while injection of MitoTEMPO showed a complete protective effect on these impairments. The histograms for CVD showed that I/R blocked the contribution of fast-conducting fibers (> 60 m/s). MitoTEMPO prevented that blockage and caused a shift in the CVD. Functional nerve damage caused by I/R can be prevented by MitoTEMPO, which can enter mitochondria, the main source of reactive oxygen species (ROS).Öğe İskemi-reperfüzyonun sıçan miyokardiyal papiller kasında oluşturduğu fonksiyon bozukluklarında mito-tempo'nun olası koruyucu etkisinin araştırılması(Necmettin Erbakan Üniversitesi Sağlık Bilimleri Enstitüsü, 2018) Akkoca, Ahmet; Dalkılıç, NizamettinKan dolaşımı ile hücre düzeyinde gerçekleşen metabolik olaylarda ihtiyaç duyulan maddelerin taşınması sağlanırken diğer taraftan da oksijenlenme ve atık maddelerin uzaklaştırılması gerçekleşir. Bu esnada herhangi bir nedenle dolaşımın durması olayına iskemi, durmasının ardından tekrar akışın başlaması ise reperfüzyon olarak adlandırılır. İskemiye maruz kalan hücrelerde fonksiyon bozukluğu ve hücrelerin ölümüne kadar giden bir dizi kimyasal olay gerçekleşirken reperfüzyonda ise oksijensiz kalan hücrelerin yeniden oksijenlenmesi ile serbest radikallerin oluşmasına sebep olan süreçler tetiklenir. Biyolojik sistemler için en önemli serbest radikal kaynağı ise mitokondri iç membranında lokalize olmuş elektron transport sistemidir. Serbest radikaller üzerine yapılan çalışmalara duyulan ilgi, birçok hastalığa sebep olduklarının anlaşılmasının ardından oldukça artmıştır. Öyle ki; diyabet, nörodejeneratif rahatsızlıklar (Parkinson, Alzheimer), kardiyovasküler hastalıklar (ateroskleroz, hipertansiyon), solunum hastalığı (astım), katarakt gelişimi, romatizmal eklem iltihabı ve türlü kanserler (kalınbağırsak kanseri, prostat, göğüs, akciğer ve mesane kanserleri) gibi pek çok hastalığa artmış serbest radikal miktarının sebep olduğu yapılan çalışmalar ile ortaya konulmuştur. Canlı sistemler oksidatif strese karşı kendi içerisinde antioksidan üretecek bir takım savunma mekanizmalarına sahip olsa da bazı durumlarda antioksidanların dışarıdan da alınması zorunlu hale gelmektedir. Bu tez çalışması kapsamında, özellikle oksidan madde oluşumu için en önemli mekanizma olan mitokondriyi doğrudan hedef alan, sentetik olarak üretilmiş ve ticari adı Mito-TEMPO olarak bilinen bir antioksidan molekülünün, iskemi-reperfüzyon sebebiyle artan serbest radikal miktarının miyokardiyal papiller kas kasılma fonksiyonu üzerinde oluşturacağı hasarlara karşı koruyucu etkisi araştırılmıştır. Oluşturulan SHAM, IR ve MT+IR gruplarına ait izometrik kasılma kayıtlarından kasılma kuvveti, kasılma süresi, yarı gevşeme süresi, +dF/dtmax ve –dF/dtmax değerleri hesaplanmış, SHAM grubuna göre iskemi-reperfüzyon uygulanan grupta farklılık gösteren ilgili parametreler, MT+IR grubunda kısmen veya tamamen SHAM grubu değerlerinde kalmıştır. Biyokimyasal değerlendirmeler için her üç gruptan da alınan kan örnekleri santrifüjlenerek kan serumları elde edilmiş ve toplam oksidan/antioksidan seviyeleri tespit edilmiştir. Buna göre; IR grubu oksidan seviyesi artmış, antioksidan seviyesi azalmış, Mito-TEMPO enjekte edilen grupta bu değerler SHAM seviyesi yakınlarında ölçülmüştür. Ayrıca tüm deney gruplarından alınan miyokardiyal papiller kas örneklerinden histolojik boyamalar sonunda görüntüler alınmış ve IR grubunda miyofibril kayıpları ile intrasitoplazmik vakuolizasyon tespit edilmiştir. Gerçekleştirilen bütün ölçüm ve analizler birlikte düşünüldüğünde iskemi-reperfüzyon ile miyokardiyal papiller kasta meydana gelen fonksiyon bozukluklarına karşı Mito-TEMPO büyük ölçüde koruyucu etki göstermiştir.Öğe Protective effect of MitoTEMPO against cardiac dysfunction caused by ischemia-reperfusion: MCAO stroke model study(Taylor & Francis Ltd, 2023) Akkoca, Ahmet; Buyukakilli, Belgin; Balli, Ebru; Gultekin, Burcu; Ozbay, Erkan; Demirbag, Hatice Oruc; Turkseven, Cagatay HanPurposeNeurological impairments are the leading cause of post-stroke mortality, while stroke-related cardiovascular diseases rank second in significance. This study investigates the potential protective effects of MitoTEMPO (2,2,6,6-tetramethyl-4-[[2-(triphenylphosphonio) acetyl] amino]-1-piperidinyloxy, monochloride, monohydrate), a mitochondria-specific antioxidant, against cardiac and neurological complications following stroke. The objective is to assess whether MitoTEMPO can be utilized as a protective agent for individuals with a high risk of stroke.Materials and methodsSeventeen-week-old male Wistar Albino rats were randomly assigned to three groups: SHAM, ischemia-reperfusion and MitoTEMPO + ischemia-reperfusion (MitoTEMPO injection 0.7 mg/kg/day for 14 days). The SHAM group underwent a sham operation, while the ischemia-reperfusion group underwent 1-h middle cerebral artery occlusion followed by three days of reperfusion. Afterwards, noninvasive thoracic electrical bioimpedance and electrocardiography measurements were taken, and sample collection was performed for histological and biochemical examinations.ResultsOur thoracic electrical bioimpedance and electrocardiography findings demonstrated that MitoTEMPO exhibited a protective effect on most parameters affected by ischemia-reperfusion compared to the SHAM group. Furthermore, our biochemical and histological data revealed a significant protective effect of MitoTEMPO against oxidative damage.ConclusionsThe findings suggest that both ischemia-reperfusion-induced cardiovascular abnormalities and the protective effect of MitoTEMPO may involve G-protein coupled receptor-mediated signaling mechanisms. This study was conducted with limitations including a single gender, a uniform age group, a specific stroke model limited to middle cerebral artery, and pre-scheduled only one ischemia-reperfusion period. In future studies, addressing these limitations may enable the implementation of preventive measures for individuals at high risk of stroke.Öğe Protective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis(Mdpi, 2023) Celen, Murat Cenk; Akkoca, Ahmet; Tuncer, Seckin; Dalkilic, Nizamettin; Ilhan, BarkinProtective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis. Peripheral nerve injuries often result in long-lasting functional deficits, prompting the need for effective interventions. MitoTEMPO (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride) is a mitochondria-targeted antioxidant that has shown protective and therapeutic effects against pathologies associated with reactive oxygen species. This study explores the utilization of MitoTEMPO as a therapeutic and protective agent for sciatic nerve crush injuries. By employing advanced mathematical approaches, the study seeks to comprehensively analyze nerve conduction parameters, nerve excitability, and the distribution of nerve conduction velocities to gauge the potential. Forty Wistar-Albino rats were randomly divided into following groups: (I) SHAM-animals subjected to sham operation and treated intraperitoneally (i.p.) with vehicle (bidistilled water) for 14 days; (II) CI (crush injury)-animals subjected to CI and treated with vehicle 14 days; (III) MiP-animals subjected to 7 days i.p. MitoTEMPO treatment before CI (0.7 mg/kg/day dissolved in vehicle) and, only vehicle for 7 days after CI, protective MitoTEMPO; and (IV) MiT-animals i.p. treated with only vehicle for 7 days before CI and 7 days with MitoTEMPO (0.7 mg/kg/day dissolved in vehicle) after CI, therapeutic MitoTEMPO. Nerve excitability parameters were measured, including rheobase and chronaxie, along with compound action potential (CAP) recordings. Advanced mathematical analyses were applied to CAP recordings to determine nerve conduction velocities and distribution patterns. The study revealed significant differences in nerve excitability parameters between groups. Nerve conduction velocity was notably reduced in the MiP and CI groups, whereas CAP area values were diminished in the MiP and CI groups compared to the MiT group. Furthermore, CAP velocity was lower in the MiP and CI groups, and maximum depolarization values were markedly lower in the MiP and CI groups compared to the SHAM group. The distribution of nerve conduction velocities indicated alterations in the composition of nerve fiber groups following crush injuries. In conclusion, postoperative MitoTEMPO administration demonstrated promising results in mitigating the detrimental effects of nerve crush injuries.
