The Effect of N-acetylcysteine on Biomarkers for Radiation-Induced Oxidative Damage in a Rat Model

Our study aimed to investigate the potential radioprotective effects of N-acetylcysteine (NAC) by comparing its biochemical effects with those of WR-2721, as a representative of clinically used radioprotectors, in preventing oxidative damage caused by gamma irradiation (single dose, 6Gy) in normal rat tissue. The rats (n=40) were divided randomly and equally into 4 groups:Control (C), Radiation (R), R+NAC (received irradiation and 1,000mg/kg NAC) and R&#65291;WR-2721 (received irradiation and 200mg/kg WR-2721) rats. Liver tissues and blood samples were harvested and utilized for reduced glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) detection. Serum and tissue GSH levels of R rats decreased compared to those of other groups (p&#60;0.01). Tissue MDA levels of R+NAC and R+WR-2721 rats decreased compared to R rats (p&#60;0.01;p&#60;0.05, respectively). Tissue MPO activities of R+NAC and R+WR-2721 rats were higher than those of R rats (p&#60;0.001). Serum MPO levels of R+WR-2721 rats were lower than those of C rats and R rats (p&#60;0.01, p&#60;0.001, respectively). In conclusion, the study suggests that the radioprotective effect against radiation-induced oxidative damage of NAC may be similar to that of WR-2721.</p

Investigation of the Possible Role of Macrophage Migration Inhibitory Factor Gene -173G/C Polymorphism ın Patients with Atherosclerosis

Purpose: Atherosclerosis is defined as an inflammatory disease that results in the formation of atherosclerotic plaques caused by the deposition of cholesterol in the arterial intima. As a result of damage to the intima layer of the vessel, foam cell formation following cholesterol accumulation and plaque development due to smooth muscle cell increase are observed. In different stages of atherosclerosis, migration of leukocytes to the vessel wall is provided by functional type chemokines; ıt was aimed to investigate the possible role of MIF -173G/C polymorphism in atherosclerosis disease depending on this function, since it has the same functional properties as chemokines. Materials and Methods: Thirty patients with 70% occlusion detected by angiography and 30 healthy individuals were included in the study. DNA isolation was performed with DNA isolation kit from blood samples taken into EDTA tubes from individuals participating in the study. Analysis of MIF -173G/C polymorphism was performed on Real Time PCR (LC480, Roche). Statistical analyzes were performed with the program STATISTICA version 13.5.0.17 (TIBCO Software Inc. (2017)). Statistical significance level p≤ 0.05 was taken in all comparisons. Results: The frequency of GG, GC and CC genotypes in the MIF -173G/C polymorphism was 55.26%, 41.18% and 66.66% in the patient group, respectively, and 44.74%, 58.82% and 33.33% in the control group. When compared with the GG genotype, it was determined that those with the GC genotype had a 0.567-fold (p=0.3367) risk of developing the disease and those with the CC genotype had a 1.6190-fold (p= 0.7038) risk of developing the disease. Conclusion: It was determined that those with the C allele in the MIF-173 G/C polymorphism pose a risk for atherosclerosis disease

Pankreas langerhans adacık hücrelerinde kalsiyum adenozin 5'trifosfataz enzim düzeylerinin deneysel diyabetik sıçan modelinde araştırılması

TEZ2036Tez (Doktora) -- Çukurova Üniversitesi, Adana, 1995.Kaynakça (s. 74-84) var.84 s. ; 30 cm.

Brassica Oleracea Var. Capitata ekstresinin antitümöral etkisinin araştırılması ve Adenozin 5'Trifosfataz enzim sistemi üzerine olan etkisi

TEZ1042Tez (Yüksek Lisans) -- Çukurova Üniversitesi, Adana, 1992.Kaynakça (s. 66-72) var.72 s. : rnk. res. ; 30 cm.

Erythrocyte membrane Na+Na^+ -K+K^+/ Mg++Mg^{++} adonesine 5' -Triphosphatase, erythrocyte superoxide dismutase and plasma malondialdehyde levels in case of glucose-6-phosphate dehydrogenase enzyme deficiency

Glukoz-6-fosfat dehidrogenaz (G6PD) enzimi, pentoz fosfat yolunun ilk ve düzenleyici anahtar enzimi olup reaksiyon neticesinde oluşan NADPH, sülfidril gruplarının korunmasında, serbest radikallerin ve peroksitlerin detoksifikasyonununda rol alır. G6PD enzim eksikliği Çukurova Bölgesinde %8.2 olarak bulunmuştur. Serbest radikaller, membran lipidlerinin ve de proteinlerin irreversibil zararından direkt sorumludur. Bu amaçla G6PD enzim eksikliğinde gözlenen hemoliz olayının fizyopatolojisine açıklık getirmek amacıyla G6PD enzim eksikliği saptanan 8 olgunun eritrosit membran enzimlerinden olan $Na^+$ -$K^+$/ $Mg^{++}$ adenozin S'-trifosfataz $Na^+$ -$K^+$/ $Mg^{++}$ ATPaz, ile süperoksit dismutaz (SOD) ve hasarın göstergesi olarak da plazma malondialdehit (MDA) düzeyleri çalışılmıştır. $Na^+$ -$K^+$/ $Mg^{++}$ ATPaz enzim aktivitesi kontrol grubunda 299±18 nmol Pi/mg protein/saat iken G6PD enzim eksikliği olan grubda 217±14 nmol Pi/mg protein/saat olarak saptanmıştır (p<0.001). SOD enzim aktivitesi kontrol ve G6PD enzim eksikliği olan grupda sırasıyla 1275±237, 646±227 U/gr Hb olarak bulunmuştur (P<0.001). MDA düzeyleri ise kontrol grubunda 1.7±1.S nmol/ml iken, G6PD enzim eksikliği olan grupda 4.4±0.5 nmol/ml olarak bulunmuştur (p<0.001). G6PD enzim eksikliği gözlenen olgularda hasarın göstergesi olan MDA düzeyleri artarken, $Na^+$ -$K^+$/ $Mg^{++}$ ATPaz ve SOD enzim düzeyleri kontrol grubuna oranla istatiksel açıdan anlamlı derecede düşük bulunmuştur.Glucose-6-phosphate dehyderogenase (G6PD) enzyme is the key enzyme of pentose phosphate pathway. The product of this reaction is NADPH which takes part in many biosynthetic reactions, detoxification of free radicals and protection of sulfhydryl groups. The frequency of G6PD deficiency is found to be 8.2% in the Çukurova region. Free radicals are responsible for irreversible depletion of lipids and proteins of membrane. For this reason, $Na^+$-$K^+$/$Mg^{++}$ Adenosin 5'Triphosphatase, ($Na^+$-$K^+$/$Mg^{++}$ ATPase), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were studied -in case of G6PD enzyme deficiency. $Na^+$-$K^+$/$Mg^{++}$ ATPase activity in control and G6PD deficiency were found to be 299+18, 217±14 nmol Pi/mg protein/hour, respectively (<0.001). SOD activity levels in the same groups were estimated as 1275±237, 646±227 U/gr Hb, respectively (pO.001). Also, MDA levels in controls and G6PD enzyme deficiency groups were found to be 1.7±1.5, 4.4±0.5 nmol/ml respectively (<0.001). According to these result, MDA levels were significantly increased in G6PD deficient group as compared to the control group

The investigation of calcium adenosine 5' triphosphatase, serum malondialdehyde and alpha tocopherol levels in experimental diabetic rat model

Bu çalışma streptezotozin (STZ) ile deneysel diyabet oluşturulan sıçanların pankreas Langerhans adacık hücrelerinde Ca++ ATPaz enziminin incelenmesi amacı ile yapılmıştır. Ayrıca çalışmalarımızı tamamlayıcı olarak lipid peroksidasyon ürünü olan malondialdahid (MDA) ve alfa tokoferol düzeyleri ölçülmüştür. Birinci aşamada deneysel diyabet modeli oluşturulmuştur. Bu amaç için sıçanlara kg başına 65 mg STZ verilmiştir. Çalışmamızın ikinci aşamasında sıçanların pankreas Langerhans adacıkları her pankreas için 7 mg kollogenaz ilave edilmek suretiyle izole edilmiştir. Çalışmanın üçüncü aşamasında adacık hücrelerinden Ca** ATPaz enzimi saflaştırılmıştır, differansiyel santrifügasyon uygulanarak mikrozom fraksiyonu izole edilmiştir. Diyabet grubu sıçanlara ait MDA düzeyleri kontrol grubu ile karşılaştırıldığında istatiksel açıdan anlamlı olarak artmıştır. Alfa tokoferol ve Ca** ATPaz düzeyleri ise diyabet grubunda istakisel açıdan anlamlı bir şekilde azalmış olarak bulunmuştur. Çalışmamızda elde ettiğimiz sonuçlarımıza göre artan lipid peroksidasyonu zar yapısının ve bütünlüğünün bozulmasına, artmış glukoz derişimi ise hücre zarlarında fosfolipid turnover'!, lipid tabakası ve yağ asidi kompozisyonunda değişimlere neden olarak Ca++ ATPaz enzimini inhibe ettiği sonucuna varılmıştır

The investigation of lipoprotein associated phospholipase A2 (Lp-PLA2) V279F single point mutation in coronary artery disease

38th Congress of the Federation-of-European-Biochemical-Societies (FEBS) -- JUL 06-11, 2013 -- Saint Petersburg, RUSSIAWOS: 000325919202180…Federat European Biochemical So