Cytotoxic effects of TEGDMA on THP-1 cells in vitro

Objective: Resin based dental materials are not stable in the oral environment and may release their components into biological media. These components may include substances such as triethylene glycol dimethacrylate (TEGDMA), which is a major co-monomer of dental resin materials. This release can trigger host immune and inflammatory responses against foreign materials, mediated by monocytes. The aim of this study was to investigate the possible cytotoxic effects of TEGDMA on human THP-1 monocytes.Material and Methods: THP-1 cells were exposed to various concentrations of TEGDMA (0.5 mM, 1 mM, 2 mM, 4 mM, or 8 mM) for 48 hours. An untreated group was used as control. The effects of TEGDMA on cell proliferation, cell viability and apoptosis were analyzed by light microscopy.Results: Cell proliferation was inhibited by 4 mM and 8 Mm TEGDMA. Increasing TEGDMA concentrations caused a decrease in cell viability. All TEGDMA concentrations used in this study had an apoptotic effect on THP-1 cells when compared with the control group.Conclusions: The dental monomer TEGDMA had an adverse effect on cell proliferation and exerted an apoptotic and toxic effect on THP-1 cells in a concentration-dependent manner

Mitochondrial DNA deletions in patients with esophagitis, Barrett’s esophagus, esophageal adenocarcinoma and squamous cell carcinoma

Background: Esophageal cancer is the eighth most common cancer globally. Esophageal adenocarcinoma (EA) and esophageal squamous-cell carcinoma (ESCC) are the two major types of esophageal cancer with poor prognosis. The mechanisms of the progression of normal esophagus to Barrett’s esophagus (BE) and EA are not fully understood. Mitochondria play a central role in generating energy, apoptosis and cell proliferation. Mutations of mitochondrial DNA (mtDNA) have been identified in many diseases including cancers. Mutations of mtDNA were investigated as a part of carcinogenesis.Objective: Our objective is to study whether the 5 kb and 7.4 kb mtDNA deletions are important in the progression of normal esophagus to BE and EA.Method: In this study, the frequency of the 5 kb and 7.4 kb deletions in mtDNA were studied in specimens ranging from nor- mal esophageal tissue to BE and EA and also from ESCC. Seventy six paraffin-embedded tissue samples were studied. Four couple primers were used.Results: Seventy-six tissue samples were analyzed total. The negative control and the positive control PCR product were detect- ed in all analyzed samples. The fusion PCR products, which represent the presence of the deletions, were not detected in any of the samples.Conclusion: We can say that, these deletions are not associated with progression of normal esophagus to BE and EA and they do not have an important role in detecting esophagitis, BE, EA, and ESSC.Keywords: Barrett's esophagus, esophageal cancer, mitochondrial DNA, 4977 bp, 7400 bp

Investigation of the Frequency of Thrombophilic Gene Mutations in Patients with Venous Thromboembolism in Eastern Turkey

Objectives: Polymorphisms in the thrombophilia genes such as Factor V Leiden (FVL), Prothrombin G20210A and methylenetetrahydrofolate reductase (MTHFR) cause genetic predisposition to thrombophilia. The regional incidence of these polymorphisms varies. The aim of our study is to evaluate the regional frequency of the most common single nucleotide polymorphisms of these thrombophilia genes. Methods: In this retrospective study, patients diagnosed with VTE in our center were included in the study. The presence of FVL, Prothrombin G20210A, MTHFR C677T, MTHFR A1298C, plasminogen activator inhibitor (PAI)-1, β-Fibrinogen, Factor XIIIA (V34L) and Glycoprotein IIIA (L33P) were investigated in blood samples obtained from the patients, and the association of genotype disorders was also evaluated. Results: Eight genotypes were analyzed in 2000 patients whose thrombophilia panel was studied in our clinic. The frequency of heterozygosity for the Factor II G20210A polymorphisms was 4,6%, the homozygosity for the Factor V Leiden polymorphism was 0,4%, for MTHFR C677T 7,6% , for MTHFR A1298C 48,1% and 15,7% , for PAI-1 38,8% and 13% , for β-Fibrinogen 30,3% and 4%, for Factor XIIIA (V34L) 23,3% and 2,4% and for Glycoprotein IIIA (L33P) 17,7% and 1,5% respectively. Conclusions: Factor V Leiden and Factor II (Prothrombin) G20210A mutations were found at a higher rate in our region compared to other regions in the west

Mitochondrial DNA deletions in patients with esophagitis, Barrett\u2019s esophagus, esophageal adenocarcinoma and squamous cell carcinoma

Background: Esophageal cancer is the eighth most common cancer globally. Esophageal adenocarcinoma (EA) and esophageal squamous-cell carcinoma (ESCC) are the two major types of esophageal cancer with poor prognosis. The mechanisms of the progression of normal esophagus to Barrett\u2019s esophagus (BE) and EA are not fully understood. Mitochondria play a central role in generating energy, apoptosis and cell proliferation. Mutations of mitochondrial DNA (mtDNA) have been identified in many diseases including cancers. Mutations of mtDNA were investigated as a part of carcinogenesis. Objective: Our objective is to study whether the 5 kb and 7.4 kb mtDNA deletions are important in the progression of normal esophagus to BE and EA. Method: In this study, the frequency of the 5 kb and 7.4 kb deletions in mtDNA were studied in specimens ranging from normal esophageal tissue to BE and EA and also from ESCC. Seventy six paraffin-embedded tissue samples were studied. Four couple primers were used. Results: Seventy-six tissue samples were analyzed total. The negative control and the positive control PCR product were detected in all analyzed samples. The fusion PCR products, which represent the presence of the deletions, were not detected in any of the samples. Conclusion: We can say that, these deletions are not associated with progression of normal esophagus to BE and EA and they do not have an important role in detecting esophagitis, BE, EA, and ESSC. DOI: https://dx.doi.org/10.4314/ahs.v19i1.43 Cite as: Keles M, Sahin I, Kurt A, Bozoglu C, Simsek G, Kabalar E, et al. Mitochondrial DNA deletions in patients with esophagitis, Barrett\u2019s esophagus, esophageal adenocarcinoma and squamous cell carcinoma. Afri Health Sci. 2019;19(1). 1671-1676. https://dx.doi.org/10.4314/ ahs. v19i1.4

Klorheksidin diglukonatın insan periferal kan kültürlerinde antioksidan enzim seviyeleri üzerine etkilerinin incelenmesi

Objectives: In the present study, it was aimed to investigate the biochemical effects of chlorhexidine digluconate (CHX) on the antioxidant enzyme levels in human peripheral blood cell cultures. Materials and Methods: The blood cultures were prepared using the blood samples obtained from 10 individuals (5 male and 5 female) who were systemically healthy and were not exposed to any toxic agent before. The cultures were exposed to different concentrations of CHX (0.05, 0.1, 0.2 ve 0.4 mmol/L). Glutation peroxidase (GPx), superoxide dismutase (SOD) and Catalase (CAT) enzyme activities were analyzed in order to evaluate the biochemical effects. Results: A dose-dependent statistically significant reduction was seen in the GPx, SOD and CAT enzyme activities in the blood cultures treated with 0.1, 0.2 ve 0.4 mmol/L concentrations of CHX. Conclusion: This is the first in vitro study investigating the effects of CHX on antioxidant enzyme levels in the human peripheral blood cultures. In conclusion, it was revealed that CHX had dose-depended cytotoxic effects by influencing the antioxidant enzyme activities in blood cells. ÖZET Amaç: Bu çalışmada, klorheksidin diglukonatın (KHG) insan periferal kan kültürlerinde antioksidan enzim seviyeleri üzerine olan biyokimyasal etkilerinin araştırılması amaçlandı. Gereç ve Yöntem: Daha önce herhangi bir toksik ajana maruz kalmamış ve sistemik olarak sağlıklı 10 bireyden (5 erkek, 5 kadın) elde edilen kan örnekleri ile kan kültürleri hazırlandı. Elde edilen kültürler farklı konsantrasyonlarda KHG (0.05, 0.1, 0.2 ve 0.4 mmol/L) ile muamele edildi. Biyokimyasal etkilerin değerlendirilmesi amacıyla glutatyon peroksidaz (GPx), süperoksit dismutaz (SOD) ve katalaz (KAT) enzim aktiviteleri incelendi. Bulgular: KHG'nin 0.1, 0.2 ve 0.4 mmol/L'luk konsantrasyonları ile muamele edilen kan kültürlerinde GPx, SOD ve CAT enzim aktivitelerinde doza bağlı istatistiksel olarak anlamlı derecede azalma izlendi (p<0.05). Sonuç: Bu çalışma, KHG'nin insan periferal kan kültürlerinde antioksidan enzim seviyeleri üzerindeki etkilerini araştıran ilk in vitro çalışmadır. Sonuç olarak, bu bileşiğin kan hücrelerindeki antioksidan enzim aktivitelerini etkilemek suretiyle doza bağlı sitotoksik etkilere sahip olduğu da ortaya konulmuştur

Tricyclic sesquiterpene copaene prevents H2O2-induced neurotoxicity

Aim: Copaene (COP), a tricyclic sesquiterpene, is present in several essential oils of medicinal and aromatic plants and has antioxidant and anticarcinogenic features. But, very little information is known about the effects of COP on oxidative stress induced neurotoxicity. Method: We used hydrogen peroxide (H2O2) exposure for 6 h to model oxidative stress. Therefore, this experimental design allowed us to explore the neuroprotective potential of COP in H2O2-induced toxicity in rat cerebral cortex cell cultures for the first time. For this purpose, methyl thiazolyl tetrazolium (MTT) and lactate dehydrogenase (LDH) release assays were carried out to evaluate cytotoxicity. Total antioxidant capacity (TAC) and total oxidative stress (TOS) parameters were used to evaluate oxidative changes. In addition to determining of 8-hydroxy-2-deoxyguanosine (8-OH-dG) levels, the single cell gel electrophoresis (SCGE or comet assay) was also performed for measuring the resistance of neuronal DNA to H2O2-induced challenge. Result: The results of this study showed that survival and TAC levels of the cells decreased, while TOS, 8-OH-dG levels and the mean values of the total scores of cells showing DNA damage increased in the H2O2 alone treated cultures. But pre-treatment of COP suppressed the cytotoxicity, genotoxicity and oxidative stress which were increased by H2O2. Conclusion: It is proposed that COP as a natural product with an antioxidant capacity in mitigating oxidative injuries in the field of neurodegenerative diseases. [J Intercult Ethnopharmacol 2014; 3(1.000): 21-28

Boric acid as a protector against paclitaxel genotoxicity

Paclitaxel (PAC) is an anticancer drug used for treatments of breast, ovarian and lung cancers. However, little data is available in the literature on its potential genotoxicity on healthy human cells. On the other hand, boron deficiency and supplementation exert important biological effects in human and animal tissues. The biological effects of dietary boron are defined, but its interaction with PAC is not known for therapeutic uses. The aim of the present study was to determine whether boric acid (BA) confer a protection against PAC genotoxicity. After the application of PAC (10 or 20 µg/l) and BA (2.5 or 5 mg/l), the genotoxic effects were assessed by sister chromatid exchange (SCE) and micronucleus (MN) tests in human blood cultures. We also analyzed nuclear division index (NDI) in peripheral lymphocytes. Our results showed that PAC significantly (P<0.05) increased the frequencies of SCEs and the formations of MNs in peripheral lymphocytes as compared to controls. PAC decreased the nuclear division index in lymphocyte cultures. Boric acid did not show cytotoxic or genotoxic effects at the concentrations tested. Furthermore, the PAC-induced increases in the genotoxicity and cytotoxicity indices were diminished by the addition of BA. The present study suggests for the first time that BA can prevent the genotoxicity of PAC on human lymphocytes