T Ü RK Bİ Y O K İM YA DE R N E Ğ İ D ERGİS İ 1976 ORJİNAL 1. ÖRNEK 2. ÖRNEK

ABSTRACT Objective: An important predictor for infant survival is birth weight. Normal fetal growth is related to various intrauterine factors. Low birth weight is thought to have relation with oxidative stress which plays an important role in reducing the birth weight. Among the paraoxonase family PON1 protects LDL and HDL from the lipid peroxidation. This is HDL associated enzyme having antioxidant property. We aimed to evaluate the arylesterase and lactonase activity of PON1 in cord blood in relation to birth weight. We hypothesized that cord blood PON1 arylesterase and lactonase activities will be compromised in neonates having low birth weight. Methods: We included 80 neonates born in our hospital irrespective of mode of delivery as 40 cases and 40 controls. PON1 arylesterase and lactonase activity were measured using spectrophotometer. Results: Serum arylesterase activity decreased significantly in low birth weight babies (p<0.05). Linear regression analysis (R=0.595) indicates significant correlation between arylesterase and birth weight. Serum lactonase activity of PON1 also gets reduced in low birth weight babies. Its linear regression analysis showed (R=0.716) suggesting significant correlation between lactonase and birth weight. Conclusion: Reduced PON1 activity can be explained on the basis of ER stress and atherogenic changes in the placental circulation. Ours is the first study in cord blood paraoxonase activities in relation to birth weight. As the sample in our study is cord blood, it is essentially a noninvasive one. Further studies are needed in this direction to assess the effect of the oxidative stress on fetus through cord blood in its long term prospective. Key Words: Paraoxonase1, arylesterase, lactonase, cord blood, low birth weight Conflict of Interest: There is no conflict of interest with any financial organization regarding the material discussed in the manuscript. ÖZE

T Ü RK Bİ Y O K İM YA DE R N E Ğ İ D ERGİS İ 1976 ORJİNAL 1. ÖRNEK 2. ÖRNEK

ABSTRACT Objective: Arterial hypertension is often associated with pathologies related with oxidative stress. Angiotensin converting enzyme (ACE) inhibitors have been used as a safe and effective treatment of hypertension and coronary heart disease. However, the significance of ACE inhibitor usage in hypertension-induced cerebrovascular and neurodegenerative diseases is still unknown. In this study, we aimed to investigate the effects of lisinopril, an ACE inhibitor, on oxidative stress and antioxidant enzyme activities in brain tissues of rats with L-NAME (N ω -Nitro-L-Arginine Methyl Ester hydrochloride) induced hypertension. Methods: Thirty-two Sprague-Dawley rats were divided into four groups: Control, L-NAME, L-NAME plus lisinopril, and only lisinopril. Hypertension was induced by oral administration of the L-NAME (75 mg/kg/day) in drinking water for 6 weeks. Rats were treated with Lisinopril (10 mg/kg/day) for six weeks. Systolic blood pressures were measured at the first, third and sixth weeks by using tail cuff method. Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxidase (GSH-Px) activity were measured from the brain tissue. Nitric oxide (NO) levels were measured from plasma. Results: Our results showed that L-NAME leads to an increase in systolic blood pressure of animals. The antihypertensive effect of lisinopril was observed. MDA level was significantly increased, and antioxidant enzymes activities were decreased in L-NAME given group (p<0.05). However, there was no statistically significant differences between the lisinopril given and other groups according to antioxidant enzymes activities (p>0.05). Conclusion: In our study, hypertension led to oxidative damage in brain tissues. Although lisinopril prevents the hypertension induced oxidative damage, direct antioxidant effect was not observed. Further studies are needed in order to gain certainty effect of lisinopril in brain tissue

T Ü RK Bİ Y O K İM YA DE R N E Ğ İ D ERGİS İ 1976 ORJİNAL 1. ÖRNEK 2. ÖRNEK Advisor to the Secretary General TOBB The Union of Chambers and Commodity Exchanges of Turkey 8 Haydarpaşa Numune Training and Research Hospital, İstanbul

ABSTRACT Objective: Cancer cells choose their metabolic pathway depending on the oxygen content and substrate concentration of the medium. A wide spectrum of therapeutic agents regulating the energy metabolism of cancer cells are in still in use. Cytosine arabinoside (Ara-C) is a pyrimidine analogue used in the treatment of acute myeloid leukemia (AML) and simvastatin is an inhibitor of HMG-CoA (3-hydroxy-3-methyl-glutaryl-CoA) reductase, which regulates cholesterol biosynthesis. Thus, this study aimed to assess the energy metabolism of HL-60 promyelocytic leukemia cells and healthy white blood cells, additionally to determine the effects of simvastatin and Ara-C, alone or in combination on the energy metabolism of these cells. Materials and Methods: Healthy white blood cells, untreated and treated HL-60 promyolocytic leukemia cell lines were incubated for 4 hours with radiolabelled glucose. Following incubation, lactate, which is one of the end products of the carbohydrate catabolism, and radiolabelled CO 2 produced by cells were collected and measured by the liquid scintillation device. In addition, glycogen consumption per hour was determined in each group. Results and Conclusion: We found that untreated HL-60 promyolocytic cells use anaerobic glycolytic pathway whereas healthy white blood cells use aerobic glycolysis for energy gain. It was concluded that combined use of Ara-C and Simvastatin might lead to significant increase in the rate of aerobic glycolysis of HL-60 promyelocytic cells and the metabolism of these leukemia cells become more similar to the metabolism of healthy white blood cells which they originate from. Key Words: Warburg effect, HL-60 cell lines, energy metabolism, simvastatin, Ara-C. Conflict of Interest: Authors declare no conflict of interest. ÖZET Amaç: Kanser hücrelerinde metabolik yönelim, ortamın oksijen içeriği ve substrat konsantrasyonuna göre düzenlenmektedir. Kanser hücresinin enerji metabolizmasının düzenlen-mesine yönelik çeşitli terapotik ajanlar halen kullanılmaktadır. Sitozin arabinosid (Ara-C) akut myeloid lösemi (AML) tedavisinde kullanılan bir pirimidin analogudur, simvastatin ise HMG-Co A (3-hidroksi-3-metil-glutaril-KoA) redüktaz inhibitörü olup kolesterol biyosentezini regüle etmektedir. Bu çalışmada, HL-60 promyelositik lösemi hücreleri ile sağlıklı beyaz kan hücrelerinin enerji metabolizmalarını belirlemek, ayrıca simvastatin ile Ara-C'nin tek tek ve kombine kullanımlarının hücrelerin enerji metabolizması üzerindeki etkilerini incelemek amaçlandı. Gereç ve Yöntemler: Bu amaçla, ilaç kullanılan ve kullanılmayan tüm HL-60 akut promyelositik lösemi hücre hatları, radyoaktif glukoz ile 4 saat inkübasyona bırakıldı. İnkübas-yon sonrası, karbonhidrat katabolizmasının son ürünlerinden laktat ve hücreler tarafından üretilen radyoaktif işaretli CO 2 toplanarak likit sintilasyon cihazında ölçüldü. Ayrıca her bir grupta saatteki glikojen tüketimi hesaplandı. Bulgular ve Tartışma: Çalışmanın sonucunda enerji eldesinde HL-60 promyelositik hücre-lerinin anaerobik glikolizi, sağlıklı lökositlerin ise aerobik glikolizi kullandıkları saptandı. Ara-C ile Simvastatinin kombine kullanımı sonucu, HL-60 promyelositik hücrelerinde aerobik glikoliz oranlarınının belirgin şekilde arttığı ve bu hücrelerin metabolizmalarını köken aldıkları beyaz kan hücrelerininkine benzer hale geldiği sonucuna varıldı