Ahu Soyocak

Effects of various agents on DNA fragmentation and telomerase enzyme activities in adenocarcinoma cell lines

Natural compounds such as resveratrol, tannic acid, and quercetin may help to treat cancer. Tamoxifen is a non-steroidal anti-estrogen drug widely used in the treatment of patients with estrogen receptor-positive breast cancer. The aim of the study was to compare the effects of these natural compounds and tamoxifen in colon adenocarcinoma (CaCo-2) and breast adenocarcinoma (MCF-7) cell lines, on telomerase enzyme activity, cell viability, number of cells and DNA fragmentation. In this study to determine telomerase enzyme activity was used PCR–ELISA kit. To determine cell viability and number of cells were used tripan blue stain. DNA fragmentation was determined by DNA ladder isolation kit. Tannic acid was more effective than resveratrol, with respect to reduction in telomerase activity, cell viability and cell count in breast adenocarcinoma. Tannic acid and tamoxifen was more effective than resveratrol and quercetin telomerase activity, cell viability and cell count in colon adenocarcinoma. Flavonoids such as resveratrol, tannic acid and quercetin which was studied on, has benefical effects on cancer therapy. These effects such as decreasing telomerase enzyme activity, cell viability and number of cells and inducing DNA fragmentation (apoptosis) must be studied for assist to develop new therapeutic pathways. There should be much more sudies in order to discover resveratrol, tannic acid and quercetin and other potential medicines.

Role of phenolic compounds in nitric oxide synthase activity in colon and breast adenocarcinoma.

Cancer chemopreventive agents are designed to reduce the incidence of tumorigenesis by intervening at one or more stages of carcinogenesis. This study aimed to determine the effects of resveratrol (RES) and tannic acid (TA), which are chemopreventive agents, on the nitric oxide synthase (NOS) levels that are effective for development of cancer in colon and breast cancer cell lines. The CaCo-2 (human colon carcinoma cell line) and MCF-7 (Michigan Cancer Foundation-7; human breast adenocarcinoma cell line) cells were grown in the laboratory. RES and TA were used to treat CaCo-2 and MCF-7 cells. Nitric Oxide Synthase Assay Kit was used to determine the NOS enzyme activity of CaCo-2 and MCF-7. Statistical differences between control and RES- and TA-treated cells were calculated using the Students t-test for double comparison. It was observed that NO activity was generally decreased in CaCo-2 and MCF-7 cells, in which RES and TA were applied. Results suggest that the phenolic compounds RES and TA have different effects on NOS enzyme activity of the colon and breast cancer cells.

Relationship between plasminogen activator inhibitor type-1 (PAI-1) gene polymorphisms and osteoporosis in Turkish women

OBJECTIVE: The development of osteoporosis is associated with several risk factors, such as genetic structures that affect bone turnover and bone mass. The impact of genetic structures on osteoporosis is not known. Plasminogen activator inhibitor type-1 regulates the bone matrix and bone balance. This study assessed the correlation between plasminogen activator inhibitor type-1 gene 4G/5G polymorphisms and osteoporosis in a population of Turkish women. METHODS: A total of 195 postmenopausal female patients who were diagnosed with osteoporosis (Group I) based on bone mineral density measurements via dual-energy x-ray absorptiometry and 90 females with no osteoporosis (Group II) were included in this study. Correlations between PAI-1 gene 4G/5G polymorphisms and osteoporosis were investigated through the identification of PAI-1 gene 4G/5G polymorphism genotypes using the polymerase chain reaction. RESULTS: No significant differences in the genotype and allele frequency of 4G/5G plasminogen activator inhibitor type-1 polymorphisms were observed between the two groups, and both groups exhibited the most frequently observed 4G5G genotype. CONCLUSION: No correlation between the development of osteoporosis in the female Turkish population and 4G/5G plasminogen activator inhibitor type-1 gene polymorphisms was observed.

Abstract 5109: Doxorubicin-induced autophagy functions as a pro-survival pathway in breast cancer cells

Breast cancer is the most common malignancy among women with about 220,000 new cases and 41,000 deaths every year in the US. Development of resistance to chemotherapeutics is the main cause of relapse and patient death; thus better understanding of the biology of the disease and mechanisms of drug resistance are urgently needed to enhance efficacy of current therapies and design novel therapeutic strategies. Recently, autophagy attracted a lot of attention because anticancer therapies, such as chemotherapy, antiestrogen therapies (i.e, tamoxifen), and radiation therapy were found to induce autophagy. Autophagy is a highly regulated lysosome-dependent degradation of misfolded proteins, macromolecules and organelles. Autophagy is induced by cellular stress including nutrient deprivation, metabolic, oxidative and hypoxic stress and may lead to either cell survival or caspase-independent autophagic cell death (type II PCD) depending on the duration and severity of the process. We have previously reported that doxorubicin, one of the most commonly used chemotherapeutic agents, induces autophagy in MCF-7 breast cancer cells. However, whether doxorubicin-induced autophagy functions as a pro-survival or pro-death pathway and the mechanism by which doxorubicin induces autopghagy was not understood. We hypothesized that doxorubicin induces autophagy as a protective survival mechanism through induction of reactive oxygen species (ROS). We found that doxorubicin predominantly induced autophagy at lower doses (0.05-0.5 uM) and apoptosis at higher doses (>1uM) in ER(+) MCF-7 and ER(−) MDA-MB-231 cells (p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5109.

The Effects of Monosodium Glutamate and Tannic Acid on Adult Rats

Background Monosodium glutamate (MSG) is a widely-used flavor enhancer and stabilizer in ready-made or packaged foods. The excessive use of MSG has been shown to increase oxidative stress in different organ systems and causes glucose metabolism disorders, obesity, and coronary diseases. Objectives In this study, the antioxidant activity of tannic acid was investigated experimentally with respect to its protective effects against overdosed MSG-induced oxidative stress in rats. The study took place in Turkey in August 2013. Methods Four groups (n = 7) of three- to four-month-old Sprague-Dawley female rats were used in this study. The first group was the control, who were administered saline. The second group received tannic acid (50 mg/kg, 3 days) intraperitoneally (i.p.). The third group received MSG (2 g/kg, 7 days) i.p., and the fourth group received both tannic acid (50 mg/kg, 3 days, pretreatment) and MSG (2 g/kg, 7 days) i.p. The animals were euthanized ten days later. Blood was collected for determining the hematological values and blood glucose levels. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were determined in the brain, liver, and kidney homogenates, and in the erythrocyte hemolysate. Histopathological examination of the brain, liver, and kidneys was conducted through hematoxylin-eosin staining. Results The data showed that the tannic acid treatment statistically decreased the MDA levels in the brain tissues of the group administered MSG and tannic acid (P < 0.001) when compared to the corresponding values of the control group. The SOD activities in the blood hemolysates of the MSG and tannic acid group increased when compared to the corresponding values for the MSG group (P < 0.01). Additionally, we found that pretreatment with tannic acid reduced blood glucose levels in comparison to the levels of the MSG group (P = 0.029). The results of our study show that tannic acid pretreatment in adult rats decreased blood glucose levels and oxidative stress. Conclusions In the literature, it was observed that short-term MSG exposure does not cause significant histological changes in the kidneys, liver, or brain cortex. These findings should be re-evaluated in additional long-term studies.

Inhibiting Telomerase Activity and Inducing Apoptosis in Cancer Cells by Several Natural Food Compounds

Today cancer is one of the most important causes of death. Therefore, researches pertinent to diagnosis, prognosis and treatment of cancer increase day by day. A large part of cancer can be treated by surgery, radiotherapy and chemotherapy. Various compounds are used for chemotherapy. Most of these anti-cancer compounds are synthetics that have toxic adverse effects. Therefore, it is crucial to reveal beneficial effects of natural compounds such as milder side effects on normal cells and potential anti-tumour effects. A great number of these compounds also have the potential to be anti-cancerogenic. Thus, importance of natural food-derived anti-cancer compound consumption has recently increased. Researches demonstrate these anti-cancerogenic features through various mechanisms. These mechanisms also include inhibition of telomerase activity and induction of apoptosis. It is presumed that these mechanisms are in interaction with each other. After giving brief information on telomeres, telomerase activity and apoptosis in this chapter, we will address the effects of several compounds on telomerase activity and apoptosis and the possible relationship they have with each other.

Induction of Apoptosis by Polyphenolic Compounds in Cancer Cells

Apoptosis, one of the main types of programmed cell death, is a kind of defense mechanism that eliminates the cells that are abnormal or not needed and plays a critical role for the development and maintenance of tissue homeostasis. Apoptosis can be triggered by various physiological and pathological stimuli. Apoptotic pathways require activation of caspases, a group destructive cystein proteases responsible for the cleavage of the key cellular proteins. Recent studies indicate that are two main apoptotic pathways, including extrinsic or death receptor pathway and intrinsic or mitochondrial pathway. Many natural compounds induce apoptosis in various cancer cells by acting through these pathways. These compounds are either antioxidants or inducers of antioxidant defense mechanism. Polyphenols (alone or in combination) are major constituents of plant-derived antioxidants that induce apoptosis by variety of mechanisms in cancer cells and reduce the risk of cancer. This chapter is focused on the effects of polyphenols such as resveratrol, quercetin and tannic acid on apoptosis in various cancers such as breast, colon and prostate cancers.

Meme kanserinde Kv 1.3 ve Kv 10.1 voltaj bağımlı potasyum kanallarının inhibisyonunun oksidatif stres üzerindeki rolü

Amac: Reaktif oksijen turevleri oksidatif stres, iyonize radyasyon maruziyeti, iskemi-reperfuzyon hasari ve kanseri iceren fizyolojik ve patolojik durumlarda artmaktadir. Calismamizda meme kanser hucrelerinin farklilasmasinda ve cogalmasinda etkili oldugu dusunulen voltaj kapili potasyum kanallarinin inhibisyonunun etkilerini gozlemek amaclandi. Yontemler: Farkli karakterlerdeki meme kanseri hucrelerine bu potasyum kanallarina ozgu siRNA’larin transfeksiyon islemi yapildi. Inkubasyon sonrasinda hucre lizatlari hazirlanarak antioksidan ve oksidan seviyeleri belirlendi. Elde edilen verilerle oksidatif stres hesaplandi. Surekli degiskenlerin normal dagilima uygunlugu Kolmogorov-Smirnov testi kullanilarak yapildi. Normal dagilim gosteren degiskenlerin gruplar arasindaki karsilastirmalari tek yonlu varyans analizi ile degerlendirildi. Coklu karsilastirmalar ise Tukey HSD testi ile gerceklestirildi. Bulgular: Kanal inhibisyonu ile invaziv olmayan karakterdeki MCF-7 hucrelerinin oksidatif stres seviyesinde dusus oldugu gozlendi. Invaziv karakterdeki MDA-MB-231 hucrelerinde ise Kv 1.3 siRNA transfekte edilen grupta oksidatif stres seviyesinde dusus belirlenirken, Kv 10.1 siRNA transfekte edilen grupta artis belirlendi. Sonuc: Voltaj kapili potasyum iyon kanallarinin inhibisyonunun kanser hucrelerinde oksidatif stres olusturabilecegi belirlenmistir. Ayrica, calismamizdaki en onemli bulgu kanser hucrelerinde voltaj bagimli potasyum kanallarinin oksidatif stres uzerinde etki yapabilecegi ve bunun hucrelerin metastatik karakteri ve iyon kanali turu ile baglantili olmasidir.

Tannik asit uygulanan meme kanseri hücrelerinde Bax proteinin değerlendirilmesi

Objectives: To compare endothelial changes after penetrating keratoplasty (PK) and deep anterior lamellar keratoplasty (DALK) in clear corneal graft. Methods: In this study, fifty six eyes undergone DALK (DALK Group) and eighty two eyes undergone PK (PK Group) due to various reasons are included. After operation at 1st, 12th, 24th and 36th month central corneal endothelial cell density (CD) and variability coefficient(CV) value examined by specular microscopy of clear graft which have not had additional surgery, greft rejection or glaucoma during follow up period were compared. Results: Endothelial cell density in DALK group were 2426p587 cell/mms 2289p579 cell/mms, 2222p541 cell/mms, 2175p521 cell/mms, in PK group were 2595p589 cell/mms, 2064p583 cell/mms, 1759p510 cell/mms 1509p494 cell/mms at 1st, 12th, 24th and 36th month respectively. Decrease in CD values were 5.9% at 12th month, 7.5% at 24th month and 9.4% at 36th month comparing with first month in DALK group. Decrease in CD values were 18.4% at 12th month, 30.2% at 24th month and 40.3% at 36th month comparing with first month in PK group. Variability coefficient (CV) values in group DALK were 23.3p6.2, 24.2p6.4, 24.2p6.1 and 24.5p5.6 at 1st,12th, 24th and 36th month respectively. Variability coefficient (CV) values in group PK were 19.6p3.4, 23.2p5.4, 25.9p6.2 and 27.5p5.7 at 1st,12th, 24th, and 36th months respectively. Conclusion: More polymegatism and more decrease in endothelial cell density with time were assessed in grafts undergone PK compared with grafts undergone DALK.Objectives: The aim of this study was to determine the effect of fracture type and angular deterioration on the outcome of calcaneal fractures. Materials and methods: Thirty-two patients (23 males, 9 females; mean age 45 years) with calcaneus fractures retrospectively reviewed. Twenty-four fractures were closed, and eight fractures were open. Bohler and Gissane angles were measured using patient’s before, and after reduction X-ray films. According to the EssexLopresti classification there were three type I, 14 type II, and 15 type III fractures. Five patients were treated with casting (Group I), 19 patients with closed reduction K-wire application (Group II), and 8 patients with plate fixation. Final clinical outcome were assessed by Maryland Foot Score. Mean follow-up period was 109 weeks.Amac: Bu calismada kalsipotriol-betametazon dipropionat ile tedavi edilen plak psoriazisli olgularda doku duzeyinde hucresel immunitenin ve serumda sitokin duzeylerinin rolunun arastirilmasi amaclandi. Gerec ve yontem: Calismaya plak tip psoriazisli 20 olgu alindi. Hastalarin tedavi oncesi ve sonrasi psoriatik lezyonlari ile saglam deriden biyopsi ve periferik kan ornekleri alindi. Bulgular: Immunohistokimyasal incelemede, CD4+, CD8+ ve CD25+ T lenfositler, tedavi oncesi lezyonlu dokuda saglam doku ve tedavi sonrasi doku ile kiyaslandiginda anlamli bir sekilde yuksekti (sirasiyla, p0.05). Sonuc: Calismamizda lezyonlu deride CD4+ ve CD8+ hucre birikimi oldugunu ve CD4+ T lenfositlerin daha hâkim hucre grubu oldugu gosterildi. Uygulanan topikal tedavinin etkinligine paralel olarak lezyonlarda duzelme olmasi ve lezyonlu bolgelerde CD4+ ve CD8+ T hucrelerinde anlamli bir azalma meydana gelmesi, Th lenfositlerin hastaligin immunopatogenezinde onemli rolunun oldugu tezini desteklemektedir. Ancak, sonuclarimiz, hastaligin kronik ozelligi ile uyumlu olarak T hucrelerin dokuda yine de yeterince kaldigini ve topikal tedavinin hastaligin aktivasyonunu engelleyemedigini gostermektedir.