Publications by authors named "Abdulgani Tatar"

44 Publications

High Expression of Stem Cell-Related Genes in Polyps with Villous Features and High-Grade Dysplasia Support Malignant Phenotype and Colorectal Carcinogenesis.

Asian Pac J Cancer Prev 2021 Aug 1;22(8):2429-2435. Epub 2021 Aug 1.

Department of Medical Genetics, Faculty of Medicine, Ataturk University, Erzurum, Turkey.

Objective: The aim of this project is to identify the differences in expression levels of stem cell related genes (SCRGs) in normal colon tissue, histopathologically staged colon polyps and colon cancer, and to explain the role of SCRGs in the formation of CC and for contributing the practical usage of SCRGs in the diagnosis and treatment of CC.

Methods: Normal colon tissue, hyperplastic polyps, histopathologically (HGD and LGD) staged tubular, tubulovillous and villous polyps and colon cancer paraffin tissue (FFPE) samples were used. Transcription factor genes (OCT4, KLF4, SOX2, MYC, NANOG, and REX1) and cell surface markers (CD133, LGR5), which are associated with embryonic stem cells, induced pluripotent stem cells, and cancer stem cells, have been selected for measuring expression levels from the selected tissues. After isolation of total RNA from FFPE tissues, SCRGs expressions were measured by RT-qPCR method.

Results: SCRGs expression differences were detected in normal-adenoma-cancer progression. A significant increase was observed in the expression of LGR5 (p: 0.01) and PROM1 (p: 0.005) genes in villous HGD polyps, LGR5 (p: 0.003) gene in G1, and LGR5 (p: 0.0002) and MYC (p: 0.002) genes in G2 stage tumor tissues. When compared with each other, a significant increase in SCRGs expression is noticeable in the formation from adenoma to cancer tissues regarding malign phenotype.

Conclusion: This study shows that the increase of SCRGs expressions occurs with high-grade dysplasia (HGD), villous features, and the malignant phenotype. Increased expression levels of LGR5, PROM1, KLF4, SOX2, and MYC in HGD and cancerous tissues support the malignant phenotype and the existence of cancer stem cells and demonstrate that they can be used to assess diagnosis and prognosis. Identification of tissue-specific SCRGs expressions will help design new therapies to control the development and progression of colonic neoplasia.
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http://dx.doi.org/10.31557/APJCP.2021.22.8.2429DOI Listing
August 2021

Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studies.

Neurochem Int 2021 Oct 19;149:105137. Epub 2021 Jul 19.

Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, UK; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden. Electronic address:

Glioblastoma (GB) is the most common and aggressive primary malignant astrocytoma correlated with poor patient survival. There are no curative treatments for GB, and it becomes resistant to chemotherapy, radiation therapy, and immunotherapy. Resistance in GB cells is closely related to their states of redox imbalance, and the role of reactive oxygen species and its impact on cancer cell survival is still far from elucidation. Boron-containing compounds, especially boric acid (BA) and borax (BX) exhibited interesting biological effects involving antibacterial, antiviral, anti-cancerogenic, anti-mutagenic, anti-inflammatory as well as anti-oxidative features. Recent studies indicated that certain boron compounds could be cytotoxic on human GB. Nevertheless, there is gap of knowledge in the literature on exploring the underlying mechanisms of anti-GB action by boron compounds. Here, we identified and compared the potential anti-GB effect of both BA and BX, and revealed their underlying anti-GB mechanism. We performed cell viability, oxidative alterations, oxidative DNA damage potential assays, and explored the inflammatory responses and gene expression changes by real-time PCR using U-87MG cells. We found that BA and BX led to a remarkable reduction in U-87MG cell viability in a concentration-dependent manner. We also found that boron compounds increased the total oxidative status and MDA levels along with the SOD and CAT enzyme activities and decreased total antioxidant capacity and GSH levels in U-87MG cells without inducing DNA damage. The cytokine levels of cancer cells were also altered. We verified the selectivity of the compounds using a normal cell line, HaCaT and found an exact opposite condition after treating HaCaT cells with BA and BX. BA applications were more effective than BX on U-87MG cell line in terms of increasing MDA levels, SOD and CAT enzyme activities, and decreasing Interleukin-1α, Interleukin-6 and Tumor necrosis factor- α (TNF- α) levels. We finally observed that anticancer effect of BA and BX were associated with the BRAF/MAPK, PTEN and PI3K/AKT signaling pathways in respect of downregulatory manner. Especially, BA application was found more favorable because of its inhibitory effect on PIK3CA, PIK3R1, PTEN and RAF1 genes. In conclusion, our analysis indicated that boron compounds may be safe and promising for effective treatment of GB.
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http://dx.doi.org/10.1016/j.neuint.2021.105137DOI Listing
October 2021

Is There an Association Between Nasal Polyposis and ADAMTS Genes Expressions?

Eurasian J Med 2021 Feb;53(1):19-21

Department of Medical Genetics, Ataturk University School of Medicine, Erzurum, Turkey.

Objective: Nasal polyposis (NP) is an inflammatory chronic disease in which polyps are located in the nose or paranasal sinuses. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) genes have roles in vascular biology, inflammation, tissue morphogenesis, and pathophysiological remodeling. Therefore, some members of the ADAMTS gene family may contribute to pathogenesis of NPs. This study aimed to detect the potential relation between NP and the expression levels of ADAMTS 5, 8, and 9 genes.

Materials And Methods: This study consisted of nasal polyp tissues from 34 patients in whom nasal polyps had been diagnosed clinically, and healthy nasal mucosal tissues from 14 controls. RNA was isolated from the nasal polyps and normal nasal mucosal tissue in each subject. The expression levels of ADAMTS 5, 8, and 9 genes in the patients and controls were detected by quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) method.

Results: The expression levels of ADAMTS 5 and 9 genes were significantly decreased in NP tissues. In contrast, the expression levels of ADAMTS 8 genes were also decreased in NP tissues, but they were not significantly different from those in the normal nasal tissues.

Conclusion: An association was detected between the expression levels of ADAMTS genes and NP. ADAMTS 5 and 9 genes may have an effect on the formation of NP.
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http://dx.doi.org/10.5152/eurasianjmed.2021.20006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7929586PMC
February 2021

A Novel Mutation of Gene in a Case of Wilson Disease.

Medicina (Kaunas) 2021 Jan 29;57(2). Epub 2021 Jan 29.

Department of Medical Biology, Faculty of Medicine, Ataturk University, 25240 Erzurum, Turkey.

Wilson disease (WD) (OMIM# 277900) is an autosomal recessive inherited disorder characterized by excess copper (Cu) storage in different human tissues, such as the brain, liver, and the corneas of the eyes. It is a rare disorder that occurs in approximately 1 in 30,000 individuals. The clinical presentations of WD are highly varied, primarily consisting of hepatic and neurological conditions. WD is caused by homozygous or compound heterozygous mutations in the gene. The diagnosis of the disease is complicated because of its heterogeneous phenotypes. The molecular genetic analysis encourages early diagnosis, treatment, and the opportunity to screen individuals at risk in the family. In this paper, we reported a case with a novel, hotspot-located mutation in WD. We have suggested that this mutation in the gene might contribute to liver findings, progressing to liver failure with a loss of function effect. Besides this, if patients have liver symptoms in childhood and/or are children of consanguineous parents, WD should be considered during the evaluation of the patients.
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http://dx.doi.org/10.3390/medicina57020123DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7912016PMC
January 2021

Mitochondrial DNA copy number may be associated with attention deficit/hyperactivity disorder severity in treatment: a one-year follow-up study.

Int J Psychiatry Clin Pract 2021 Mar 8;25(1):37-42. Epub 2021 Feb 8.

Department of Child and Adolescent Psychiatry, University of Health Sciences Faculty of Medicine, Trabzon, Turkey.

Objective: Studies on etiopathogenesis of attention deficit/hyperactivity disorder (ADHD) are increasingly focussing on mitochondrial dysfunction. Children diagnosed with ADHD who had significantly higher mitochondrial DNA (mtDNA) copy numbers than healthy children in our first study were re-examined in 1-year follow-up to investigate effects of severity and treatment of ADHD on mtDNA.

Methods: Twenty-eight patients who participated in previous study were included in this follow-up study. Patients were equally divided into two groups according to whether they had been receiving treatment. Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version, and Conners Parent Rating Scale (CPRS) were used. Polymerase chain reaction was performed.

Results: Means of the first and second mtDNA copy were similar in all patients. mtDNA copy numbers did not change between two measurements in treated and non-treated groups. There was a correlation between CPRS ADHD index and inattention scores and mtDNA copy number in treated group. mtDNA copy number did not change in patients with ADHD over a period of 1 year regardless of treatment.

Conclusions: There may be a relationship between decreased ADHD severity with treatment and positive effects of mitochondrial functions. Mitochondrial dysfunction may play a role in pathophysiology of ADHD.KEY POINTSThis was the first study to follow up ADHD patients in order to investigate mitochondrial dysfunction by measuring mtDNA copy numbers 1 year after the initial measurements.mtDNA copy number, one of the best markers of mitochondrial dysfunction, did not change in ADHD patients over a period of 1 year regardless of treatment.Mitochondrial dysfunction may play a role in the pathophysiology of ADHD, where it may be involved with or without treatment.In the treated group, there was an association between decreased ADHD severity and reduced mtDNA copy numbers.There may be a relationship between decreased ADHD severity with treatment and the positive effects of mitochondrial functions.
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http://dx.doi.org/10.1080/13651501.2021.1879158DOI Listing
March 2021

Glycyl-L-Prolyl-L-Glutamate Pseudotripeptides for Treatment of Alzheimer's Disease.

Biomolecules 2021 01 19;11(1). Epub 2021 Jan 19.

Science for Life Laboratory, KTH-Royal Institute of Technology, 24075 Stockholm, Sweden.

So far, there is no effective disease-modifying therapies for Alzheimer's Disease (AD) in clinical practice. In this context, glycine-L-proline-L-glutamate (GPE) and its analogs may open the way for developing a novel molecule for treating neurodegenerative disorders, including AD. In turn, this study was aimed to investigate the neuroprotective potentials exerted by three novel GPE peptidomimetics (GPE1, GPE2, and GPE3) using an in vitro AD model. Anti-Alzheimer potentials were determined using a wide array of techniques, such as measurements of mitochondrial viability (MTT) and lactate dehydrogenase (LDH) release assays, determination of acetylcholinesterase (AChE), α-secretase and β-secretase activities, comparisons of total antioxidant capacity (TAC) and total oxidative status (TOS) levels, flow cytometric and microscopic detection of apoptotic and necrotic neuronal death, and investigating gene expression responses via PCR arrays involving 64 critical genes related to 10 different pathways. Our analysis showed that GPE peptidomimetics modulate oxidative stress, ACh depletion, α-secretase inactivation, apoptotic, and necrotic cell death. In vitro results suggested that treatments with novel GPE analogs might be promising therapeutic agents for treatment and/or or prevention of AD.
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http://dx.doi.org/10.3390/biom11010126DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7835747PMC
January 2021

Safety Assessments of Nickel Boride Nanoparticles on the Human Pulmonary Alveolar Cells by Using Cell Viability and Gene Expression Analyses.

Biol Trace Elem Res 2021 Jul 9;199(7):2602-2611. Epub 2020 Sep 9.

Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, UK.

Nickel boride is generally used in the steel industry as a melting accelerator due to its feature of creating a protective and stable attribute at high temperatures. It is also used to improve the hardenability of the steel with boron addition in the production. Thus, safety studies and biocompatibility analysis of nickel boride should be performed comprehensively to understand the limitations of use in various areas. In the present study, nickel boride nanoparticles (NiB NPs) were synthesized by a single-step method and molecule characterizations were performed via the use of X-ray diffraction analysis (XRD), transmission electron microscopy (TEM), scanning electron microscopy (SEM), and energy dispersive X-ray (EDX) analyses. Cytotoxicity properties of NiB NPs were identified on human pulmonary alveolar epithelial cells (HPAEpiC) by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), neutral red (NR), and lactate dehydrogenase (LDH) assays. Illumina human ht-12 v4.0 whole-genome microarray analysis was conducted to investigate NiB NPs effects on gene expression regulations of HPAEpiC cells. The database for annotation, visualization, and integrated discovery (DAVID) analysis was performed to reveal the relationship between NiB NP application and cellular pathway alterations. According to cytotoxicity analysis, the IC value for NiB NP application was found as 81.99 mg/L concentration. Microarray analysis of NiB NP application was shown for the first time that 693 gene expression changes (FC ≥ 2) occurred significantly over 40.000 gene probes and NiB NPs were observed to affect microtubule regulation, centrosome organization, and phosphoprotein synthesis.
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http://dx.doi.org/10.1007/s12011-020-02374-7DOI Listing
July 2021

Mitochondrial DNA Copy Number is Associated with Attention Deficit Hyperactivity Disorder.

Psychiatr Danub 2020 ;32(2):168-175

Department of Child and Adolescent Psychiatry, Ankara City Hospital, 06000 Ankara, Turkey,

Background: Attention deficit hyperactivity disorder (ADHD) is the most common psychiatric disorder in children. Several hypotheses have been proposed to explain its etiology. Mitochondrial dysfunction (MD) is suggested to be one of the causes of Attention Deficit Hyperactivity Disorder. The objective of the study was to evaluate the relationship between MD and ADHD by investigating mitochondrial DNA (mtDNA) levels from peripheral blood leukocytes, one of the best biomarkers of mitochondrial dysfunction.

Subjects And Methods: This study included 56 children aged 6-16 years who were diagnosed with ADHD for the first time and 56 age- and sex-matched children without ADHD. Real-time PCR was performed to determine the relative mtDNA copy number in each study participant.

Results: The mean mtDNA copy number of the case group was 57.623±24.827 and that of the control group was 44.204±18.926 (p=0.002). The mtDNA copy number of the case group was higher than that of the control group. Results of ROC curve analysis provided a mtDNA cutoff value of 45.

Conclusion: Significantly higher mtDNA copy number in ADHD group may suggest mitochondrial dysfunction in the etiopathogenesis of ADHD.
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http://dx.doi.org/10.24869/psyd.2020.168DOI Listing
September 2020

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

Afr Health Sci 2019 Mar;19(1):1671-1676

Department of Medical Genetics, Ataturk University Medical Faculty, Erzurum, Turkey.

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 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.
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http://dx.doi.org/10.4314/ahs.v19i1.43DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6531945PMC
March 2019

Microarray assisted toxicological investigations of boron carbide nanoparticles on human primary alveolar epithelial cells.

Chem Biol Interact 2019 Feb 24;300:131-137. Epub 2019 Jan 24.

Department of Medical Genetics, Medical Faculty, Atatürk University, Erzurum, Turkey.

It is important to understand the adverse effects of nanoparticles on human health and to prepare risk reports for widely used nanoscale materials. Synthesis, characterization and cytotoxicity evaluation of BC nanoparticles were performed on HPAEpiC since, first encounter with nanoparticles would generally happen through lung by inhaling chemicals. BC nanoparticles were synthesized via chemical vapor deposition techniques and characterized by using transmission electron microscope (TEM), scanning electron microscope (SEM) and X-ray crystallography (XRD). 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT), lactate dehydrogenase (LDH) and neutral red (NR) tests were used to analyze cell viability and cytotoxicity against nanoparticles exposure. Microarray analysis was used to discover whole genome effects of BC NPs on gene expressions changes of HPAEpiC cells. Then, the database for annotation, visualization and integrated discovery (DAVID) analysis was performed to understand relationships between gene pathways and nanoparticle exposure. Finally, cytotoxicity analysis revealed that IC value for boron carbide (BC) nanoparticles was 202.525 mg/L. According to microarray analysis 32 genes expression change significantly (FC ≥ 2) over 40,000 genes scanning. The gene pathways analysis showed that boron carbide (BC) nanoparticles mostly affect amino acid biosynthesis process, TGF-beta signaling pathway and developmental proteins regulation. In conclusion, our results supported for the first time that boron carbide (BC) nanoparticles could be used as a safe nanomaterial in both pharmacological and medical applications.
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http://dx.doi.org/10.1016/j.cbi.2019.01.021DOI Listing
February 2019

Synthesis, characterization and cytotoxicity of boron nitride nanoparticles: emphasis on toxicogenomics.

Cytotechnology 2019 Feb 14;71(1):351-361. Epub 2019 Jan 14.

Department of Biology, Faculty of Arts and Sciences, Atatürk University, Erzurum, Turkey.

Nanotechnology is increasingly developing area including more than 700 commercial products such as clothing, food preparation, cosmetics, mechanics, electronics and also health industry. People generally contact with nanoparticles by inhaling from air. Thus, it is becoming important issue to understand harmful effects of nanoparticles on human health and prepare risk reports for common nano-sized materials. In this paper, synthesis, characterization and cytotoxicity evaluation of boron nitride (BN) nanoparticles were performed on human primary alveolar epithelial cells (HPAEpiC) since, main exposure to nanoparticles would generally happen through lung via inhalation. Chemically synthetized BN nanoparticles were characterized by using X-ray crystallography, transmission electron microscope, scanning electron microscope and energy-dispersive X-ray spectroscopy techniques. 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide, neutral red and lactate dehydrogenase release assays were used to analyze cytotoxicity after nanoparticles exposure. Whole genome microarray analysis was used to find out the effects of BN NPs on gene expressions of HPAEpiC cells. Finally, the database for annotation, visualization and integrated discovery analysis was used to reveal relationships between different cellular pathways and nanoparticle exposure. According to cytotoxicity analysis LC value for BN nanoparticles was 125.051 mg/L. Microarray results showed that 2159 genes expression change (FC ≥ 2) significantly over 40,000 genes analysis. When the gene pathways were analyzed, it was seemed that BN nanoparticles mostly affect cell cycle, cell-cell interactions, cancer affecting genes and signal transduction. In a conclusion, our results supported for the first time that BN nanoparticles could be used as a safe nanomaterial in both pharmacological and medical applications.
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http://dx.doi.org/10.1007/s10616-019-00292-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368500PMC
February 2019

Becker's myotonia: novel mutations and clinical variability in patients born to consanguineous parents.

Acta Neurol Belg 2018 Dec 26;118(4):567-572. Epub 2018 Feb 26.

Department of Medical Genetics, Ataturk University School of Medicine, 25240, Erzurum, Turkey.

Myotonia congenita is an inherited muscle disease present from childhood that is characterized by impaired muscle relaxation after contraction resulting in muscle stiffness; moreover, skeletal striated muscle groups may be involved. Myotonia congenita occurs due to chloride (Cl) channel mutations that reduce the stabilizing Cl conductance, and it is caused by mutations in the CLCN1 gene. This paper describes four patients from two different healthy consanguineous Turkish families with muscle stiffness and easy fatigability. A genetic investigation was performed. Mutation analyses showed a homozygous p.Tyr150* (c.450C > A) mutation in patients 1, 2 and 3 and a homozygous p.Leu159Cysfs*11 (c.475delC) mutation in patient 4 in the CLCN1 gene. These mutations have never been reported before and in silico analyses showed that the mutations were disease causing. They may be predicted to cause nonsense-mediated mRNA decay. Our data expand the spectrum of CLCN1 mutations and provide insights for genotype-phenotype correlations of myotonia congenita.
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http://dx.doi.org/10.1007/s13760-018-0893-0DOI Listing
December 2018

Memantine-derived drugs as potential antitumor agents for the treatment of glioblastoma.

Eur J Pharm Sci 2017 Nov 30;109:402-411. Epub 2017 Aug 30.

Department of Pharmacy, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.

Glioblastoma is one of the most aggressive malignant primary brain cancer in adults. To date, surgery, radiotherapy and current pharmacological treatments are not sufficient to manage this pathology that has a high mortality rate (median survival 12-15months). Recently, anticancer multi-targeted compounds have attracted much attention with the aim to obtain new drugs able to hit different biological targets that are involved in the onset and progression of the disease. Here, we report the synthesis of novel memantine-derived drugs (MP1-10) and their potential antitumor activities in human U87MG glioblastoma cell line. MP1-10 were synthetized joining memantine, which is a NMDA antagonist, to different histone deacetylase inhibitors to obtain one molecule with improved therapeutic efficacy. Biological results indicated that MP1 and MP2 possessed more potent anti-proliferative effects on U87MG cells than MP3-10 in a dose-dependent manner. MP1 and MP2 induced significant cell death by apoptosis characterized by apoptotic morphological changes in Hoechst staining. Both drugs also exhibited non-genotoxic and only mild cytotoxic effects in human whole blood cells. However, only MP1, showing good chemico-physical properties (solubility, LogP) and enzymatic stabilities in gastric and intestinal fluids, can be considered a suitable candidate for in vivo pharmacokinetic studies.
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http://dx.doi.org/10.1016/j.ejps.2017.08.030DOI Listing
November 2017

Toxicogenomic responses of human alveolar epithelial cells to tungsten boride nanoparticles.

Chem Biol Interact 2017 Aug 27;273:257-265. Epub 2017 Jun 27.

Department of Biology, Faculty of Arts and Sciences, Atatürk University, Erzurum, Turkey.

During the recent years, microarray analysis of gene expression has become an inevitable tool for exploring toxicity of drugs and other chemicals on biological systems. Therefore, toxicogenomics is considered as a fruitful area for searching cellular pathways and mechanisms including cancer, immunological diseases, environmental responses, gene-gene interactions and chemical toxicity. In this work, we examined toxic effects of Tungsten Borides NPs on gene expression profiling of the human lung alveolar epithelial cells (HPAEpiC). In line with this purpose, a single crystal of tungsten boride (mixture of WB and WB) nanoparticles was synthesized by means of zone melting method, and characterized via using X-ray crystallography (XRD), transmission electron microscope (TEM), scanning electron microscope (SEM) and energy-dispersive X-ray spectroscopy (EDX) techniques. Cell viability and cytotoxicity were determined by 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT), neutral red (NR) and lactate dehydrogenase (LDH) release tests. The whole genome microarray expression analysis was performed to find out the effects of WB and WB NPs mixture on gene expression of the HPAEpiC cell culture. 123 of 40,000 gene probes were assigned to characterize expression profile for WB/W2B NPs exposure. According to results; 70 genes were up-regulated and 53 genes were down-regulated (≥2 fold change). For further investigations, these genes were functionally classified by using DAVID (The Database for Annotation, Visualization and Integrated Discovery) with gene ontology (GO) analysis. In the light of the data gained from this study, it could be concluded that the mixture of WB/W2B NPs can affect cytokine/chemokine metabolism, angiogenesis and prevent migration/invasion by activating various genes.
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http://dx.doi.org/10.1016/j.cbi.2017.06.027DOI Listing
August 2017

Myhre syndrome with novel findings: bilateral congenital cortical cataract, bilateral papilledema, accessory nipple, and adenoid hypertrophy.

Clin Dysmorphol 2018 Jan;27(1):12-14

Department of Medical Genetics, Ataturk University Medical Faculty, Erzurum, Turkey.

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http://dx.doi.org/10.1097/MCD.0000000000000188DOI Listing
January 2018

Molecular genetic and biochemical responses in human airway epithelial cell cultures exposed to titanium nanoparticles in vitro.

J Biomed Mater Res A 2017 Jul 17;105(7):2056-2064. Epub 2017 May 17.

Faculty of Science Department of Biology, Atatürk University, Erzurum, TR-25240, Turkey.

Titanium nanoparticles (NPs) have very wide application areas such as paint, cosmetics, pharmaceuticals, and biomedical applications. And, to translate these nanomaterials to the clinic and industrial domains, their safety needs to be verified, particularly in terms of genotoxicity and cytotoxicity. Therefore, in this study, we aimed to investigate of cytotoxicity and changes in gene expression profiles influenced by commonly titanium (as titanium carbide, titanium carbo-nitride, titanium (II) oxide, titanium (III) oxide, titanium (IV) oxide, titanium nitride, titanium silicon oxide) NPs in human alveolar epithelial (HPAEpiC) and pharynx (HPPC) cell lines in vitro since inhalation is an important pathway for exposure to these NPs. HPAEpiC and HPPC cells were treated with titanium (0-100 µg/mL), NPs for 24 and 48 h, and then cytotoxicity was detected by, [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT), uptake of neutral red (NR) and lactate dehydrogenase (LDH) release assays, while genotoxicity was also analyzed by cDNA array - RT-PCR assay. According to the results of MTT, NR and LDH assays, all tested NPs induced cytotoxicity on both HPAEpiC and HPPC cells in a time- and dose-dependent manner. Determining and analyzing the gene expression profiles of HPAEpiC and HPPC cells, titanium NPs showed more changes in genes related to DNA damage or repair, oxidative stress, and apoptosis. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2056-2064, 2017.
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http://dx.doi.org/10.1002/jbm.a.35994DOI Listing
July 2017

Correlation with Platelet Parameters and Genetic Markers of Thrombophilia Panel (Factor II g.20210G>A, Factor V Leiden, MTHFR (C677T, A1298C), PAI-1, β-Fibrinogen, Factor XIIIA (V34L), Glycoprotein IIIa (L33P)) in Ischemic Strokes.

Neuromolecular Med 2016 Jun 7;18(2):170-6. Epub 2016 Mar 7.

Department of Medical Genetics, Ataturk University Medical Faculty, 25240, Erzurum, Turkey.

An important type of arterial thrombosis, ischemic stroke is associated with increased mortality risk, severe disability and life quality impairment. In this study, we analyzed mean platelet volume, platelet count values and genetic thrombophilia markers of patients who have ischemic stroke history and searched the relationship with genetic predisposition of ischemic strokes and platelet parameters. A retrospective, clinical trial was performed by reviewing the ischemic stroke history (except cryptogenic events) of 599 patients and 100 controls. The results of the genetic thrombophilia panel were used to classify the study group and control group into low and high risk for thrombophilia groups. The high-risk group included patients homozygous/heterozygous for Factor II g.20210G>A or Factor V Leiden mutations with/without any other polymorphism. The low-risk group included patients heterozygous or homozygous for MTHFR (C677T, A1298C), PAI-1, β-fibrinogen, Factor XIIIA (V34L) and glycoprotein IIIa (L33P) polymorphisms or negative in terms of both mutations and polymorphisms. The results of study showed us that high-risk group mutations are important risk factors for ischemic stroke but low-risk group polymorphisms are not significant. According to platelet parameters, although there was a significant difference between MPV and PLT values of ischemic stroke and control group, thrombophilia mutations and polymorphisms have not a significant effect on MPV and PLT values in ischemic stroke patients.
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http://dx.doi.org/10.1007/s12017-016-8386-xDOI Listing
June 2016

The Relationship Between Endothelial Nitric Oxide Synthase Gene (NOS3) Polymorphisms, NOS3 Expression, and Varicocele.

Genet Test Mol Biomarkers 2016 Apr 11;20(4):191-6. Epub 2016 Feb 11.

2 Department of Medical Genetics, Ataturk University Medical Faculty , Erzurum, Turkey .

Background: Varicocele is an abnormal enlargement of the pampiniform venous plexus in the scrotum. Varicocele is the most common cause of secondary male infertility. Nitric oxide (NO), which has a role on varicocele pathophysiology, is synthesized by endothelial nitric oxide synthase gene (NOS3).

Objective: In our study, we aimed to explain the relationship between varicocele, three common NOS3 polymorphisms (T-786C, G894T, 4b/a), and NOS3 mRNA expression levels.

Methods: We investigated NOS3 T-786C, G894T, and 4b/a polymorphisms in 102 patients with varicocele and 100 healthy controls. Twenty-four patients and 17 controls were chosen for expression studies based on polymorphism subgroupings. Subgroup 1 includes patients who have no minor allele polymorphisms, and subgroups 2, 3, and 4 have T-786C, G894T, and 4b/a polymorphisms, respectively.

Results: The 4b/a polymorphism demonstrated significantly elevated levels in both allele and genotype analysis in the control group compared to the patient group. The G894T polymorphism was statistically elevated for genotypic frequencies in the patient group compared to the control group, but this finding did not extend to allelic frequencies. There were no statistically significant differences in either the allelic or genotypic frequencies between patients and control groups for the T-786C polymorphism. When patient and control expression levels were compared without considering the subgroups, the NOS3 expression level was found to be statistically higher in the patient group. There were no statistically significant differences in the patient and control group expression levels when stratified by subgroup, nor was there any effect of the polymorphisms under study on expression levels.

Conclusions: The 4b/a polymorphism may have a protective effect for varicocelem and G894T polymorphism may contribute to varicocele occurrence by lowering the level of NO. The higher NOS3 expression levels in the patient group may be a kind of dilator compensatory mechanism to protect vascular anatomy in varicocele.
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http://dx.doi.org/10.1089/gtmb.2015.0294DOI Listing
April 2016

Mitochondrial DNA deletions in patients with chronic suppurative otitis media.

Eur Arch Otorhinolaryngol 2016 Sep 30;273(9):2473-9. Epub 2015 Nov 30.

Department of Medical Genetics, Faculty of Medicine, Ataturk University, Erzurum, Turkey.

The aim of this study was to investigate the 4977 and 7400 bp deletions of mitochondrial DNA in patients with chronic suppurative otitis media and to indicate the possible association of mitochondrial DNA deletions with chronic suppurative otitis media. Thirty-six patients with chronic suppurative otitis media were randomly selected to assess the mitochondrial DNA deletions. Tympanomastoidectomy was applied for the treatment of chronic suppurative otitis media, and the curettage materials including middle ear tissues were collected. The 4977 and 7400 bp deletion regions and two control regions of mitochondrial DNA were assessed by using the four pair primers. DNA was extracted from middle ear tissues and peripheral blood samples of the patients, and then polymerase chain reactions (PCRs) were performed. PCR products were separated in 2 % agarose gel. Seventeen of 36 patients had the heterozygote 4977 bp deletion in the middle ear tissue but not in peripheral blood. There wasn't any patient who had the 7400 bp deletion in mtDNA of their middle ear tissue or peripheral blood tissue. The patients with the 4977 bp deletion had a longer duration of chronic suppurative otitis media and a higher level of hearing loss than the others (p < 0.01). Long time chronic suppurative otitis media and the reactive oxygen species can cause the mitochondrial DNA deletions and this may be a predisposing factor to sensorineural hearing loss in chronic suppurative otitis media. An antioxidant drug as a scavenger agent may be used in long-term chronic suppurative otitis media.
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http://dx.doi.org/10.1007/s00405-015-3839-7DOI Listing
September 2016

Astrocyte/neuron ratio and its importance on glutamate toxicity: an in vitro voltammetric study.

Cytotechnology 2016 Aug 6;68(4):1425-33. Epub 2015 Oct 6.

Department of Medical Pharmacology, Faculty of Medicine, Erzincan University, Erzincan, Turkey.

The purpose of this study was to clarify the relationship between neuron cells and astrocyte cells in regulating glutamate toxicity on the 10th and 20th day in vitro. A mixed primary culture system from newborn rats that contain cerebral cortex neurons cells was employed to investigate the glutamate toxicity. All cultures were incubated with various glutamate concentrations, then viability tests and histological analyses were performed. The activities of glutamate transporters were determined by using in vitro voltammetry technique. Viable cell number was decreased significantly on the 10th day at 10(-7) M and at 10(-6) M glutamate applications, however, viable cell number was not decreased at 20th day. Astrocyte number was increased nearly six times on the 20th day as compared to the 10th day. The peak point of glutamate reuptake capacity was about 2 × 10(-4) M on the 10th day and 10(-3) M on the 20th day. According to our results, we suggested that astrocyte age was important to maintain neuronal survival against glutamate toxicity. Thus, we revealed activation or a trigger point of glutamate transporters on astrocytes due to time since more glutamate was taken up by astrocytes when glutamate transporters on the astrocyte were triggered with high exogenous glutamate concentrations. In conclusion, the present investigation is the first voltammetric study on the reuptake parameters of glutamate in vitro.
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http://dx.doi.org/10.1007/s10616-015-9902-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960189PMC
August 2016

Guaiazulene biochemical activity and cytotoxic and genotoxic effects on rat neuron and N2a neuroblastom cells.

J Intercult Ethnopharmacol 2015 Jan-Mar;4(1):29-33. Epub 2015 Jan 3.

Department of Biology, Faculty of Science, Ataturk University, Erzurum, Turkey.

Aim: Neuroblastoma (NB)cells are often used in cancer researches such as glioblastoma cells since they have the potential of high mitotic activity, nuclear pleomorphism, and tumor necrosis. Guaiazulene (GYZ 1,4-dimethyl-7-isopropylazulene)is present in several essential oils of medicinal and aromatic plants. Many studies have reported the cytotoxic effect of GYZ; however, there are no studies that compare such effects between cancer cell lines and normal human cells after treatment with GYZ.

Materials And Methods: In this study, we aimed to describe in vitro antiproliferative and/or cytotoxic properties (by 3-[4,5 dimetylthiazol -2-yl]-2,5 diphenlytetrazolium bromide [MTT] test), oxidative effects (by total antioxidant capacity [TAC] and total oxidative stress [TOS] analysis)and genotoxic damage potentials (by single cell gel electrophoresis)of GYZ.

Result: The results indicated that GYZ have anti-proliferative activity suppressing the proliferation of neuron and N2a-NB cells at high doses. In addition, GYZ treatments at higher doses led to decreases of TAC levels and increases of TOS levels in neuron and N2a-NB cells. On the other hand, the mean values of the total scores of cells showing DNA damage were not found different from the control values.

Conclusion: From this study, it is observed that GYZ has in vitro cytotoxic activity against neuron and N2a-NB cells.
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http://dx.doi.org/10.5455/jice.20141124062203DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566767PMC
September 2015

Vici syndrome in siblings born to consanguineous parents.

Am J Med Genet A 2016 Jan 23;170A(1):220-5. Epub 2015 Sep 23.

Department of Medical Genetics, Ataturk University, Erzurum, Turkey.

Vici syndrome (OMIM 242840) is a rare syndrome and since its initial description by Vici et al. [1988], only 29 cases have been reported. We describe two brothers from healthy consanguineous Turkish parents with psychomotor delay, congenital bilateral cataracts, high palate, long philtrum, micrognathia, fair hair, and skin. They both had general hypotonia and elevated muscle enzymes. Magnetic resonance imaging (MRI) of the brain confirmed agenesis of corpus callosum in both patients. Secundum type atrial septal defect (in Patient 1) and mild mitral, tricuspid, and pulmonary insufficiency (in Patient 2) were detected by echocardiographic examination. Immunological studies were normal, as were chromosome karyotype analyses (46, XY). Both children had bilateral cutaneous syndactyly between second and third toes and also bilateral sensorineural hearing loss. Patient 1 had poor feeding and regurgitation necessitating a feeding tube; mild laryngomalacia was subsequently detected by bronchoscopy. Mutation analysis in patient 2 showed a homozygous p.R2483* (c.7447C > T) mutation in EPG5 gene. We report a summary of the clinical findings in our patients and 29 cases from the literature.
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http://dx.doi.org/10.1002/ajmg.a.37398DOI Listing
January 2016

The in vitro protective effect of salicylic acid against paclitaxel and cisplatin-induced neurotoxicity.

Cytotechnology 2016 Aug 22;68(4):1361-7. Epub 2015 Jul 22.

Department of Biology, Faculty of Science, Atatürk University, Erzurum, Turkey.

Paclitaxel (PAC) and cisplatin (CIS) are two established chemotherapeutic drugs used in combination for the treatment of various solid tumors. However, the usage of PAC and CIS are limited because of the incidence of their moderate or severe neurotoxic side effects. In this study, we aimed to assess the protective role of salicylic acid (SA) against neurotoxicity caused by PAC and CIS. For this purpose, newborn Sprague Dawley rats were decapitated in sterile atmosphere and primary cortex neuron cultures were established. On the 10th day SA was added into culture plates. PAC and CIS were added on the 12th day. The cytotoxicity was determined by using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Oxidative alterations were assessed using total antioxidant capacity and total oxidative stress assays in rat primary neuron cell cultures. It was shown that both concentrations of PAC and CIS treatments caused neurotoxicity. Although SA decreased the neurotoxicity by CIS and PAC, it was more effective against the toxicity caused by CIS rather than the toxicity caused by PAC. In conclusion it was clearly revealed that SA decreased the neurotoxic effect of CIS and PAC in vitro.
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http://dx.doi.org/10.1007/s10616-015-9896-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960183PMC
August 2016

Genotoxicity in primary human peripheral lymphocytes after exposure to lithium titanate nanoparticles in vitro.

Toxicol Ind Health 2016 Aug 31;32(8):1423-1429. Epub 2014 Dec 31.

Department of Physics, K. K. Education Faculty, Atatürk University, Erzurum, Turkey.

Lithium titanate (LiTiO) nanoparticles (LTT NPs; <100 nm) are widely used in battery technology, porcelain enamels, and ceramic insulating bodies. With the increased applications of LTT NPs, the concerns about their potential human toxicity effects and their environmental impact were also increased. However, toxicity data for LTT NPs relating to human health are very limited. Therefore, the purpose of this study was to evaluate whether LTT NPs are able to induce genetic damage in human peripheral lymphocytes in vitro when taking into consideration that DNA damage plays an important role in carcinogenesis. With this aim, the chromosome aberrations (CA), sister chromatid exchanges (SCE), and micronucleus (MN) assays were used as genotoxicity end points. Human peripheral lymphocytes obtained from five healthy male volunteers were exposed to LTT NPs at final dispersed concentrations ranging from 0 to 1000 μg/mL for 72 h at 37°C. The obtained results indicated that LTT NPs compound did not induce DNA damage in human peripheral lymphocytes as depicted by CA/cell, SCE/cell, and MN/1000 cell values in all concentrations tested. In summary, our results revealed that exposure to LTT NPs is not capable of inducing DNA lesions in human peripheral lymphocytes for the first time.
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http://dx.doi.org/10.1177/0748233714562624DOI Listing
August 2016

Cytotoxicity and genotoxicity of zingiberene on different neuron cell lines in vitro.

Cytotechnology 2015 Dec 7;67(6):939-46. Epub 2014 May 7.

Department of Biology, Faculty of Science, Atatürk University, Erzurum, Turkey.

The main objective of this study is to investigate the cytotoxic, genotoxic and antioxidant properties of zingiberene (ZBN) in an in vitro rat brain cell culture study. The cytotoxic effect was determined against the rat neuron and N2a neuroblastoma (N2a-NB) cell lines using the 3,(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, while the antioxidant activity was assessed using the total antioxidant capacity (TAC) and total oxidative stress (TOS) assays. The effects on DNA damage were also evaluated in this study by the single cell gel electrophoresis assay. The results indicated that ZBN has an anti-proliferative activity suppressing the proliferation of N2a-NB cells at concentrations over 50 mg L(-1) and neuron cells at concentrations over 150 mg L(-1). In addition, ZBN treatments at higher doses (≤50 mg L(-1)) led to increases of TOS levels in N2a-NB cell cultures. However 25 mg L(-1) of ZBN treatment caused increases of TAC levels in cultured neuron and N2a-NB cell cultures while ZBN at doses of 10-400 mg L(-1) did not increase the number of total damage score in both cell lines. This study clearly indicates that ZBN has a significant potential to be used as a natural anticancer agent in cultured N2a-NBs.
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http://dx.doi.org/10.1007/s10616-014-9729-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4628918PMC
December 2015

Holoprosencephaly: ZIC2 mutation in a case with panhypopituitarism.

J Pediatr Endocrinol Metab 2014 Jul;27(7-8):777-81

Background: Holoprosencephaly (HPE), the most common malformation of the brain, results from failed or incomplete separation of the embryonic forebrain (prosencephalon). HPE occurs in approximately 1 in 250 embryos and in about 1 in 10,000 births. It is etiologically heterogeneous, and may be caused by cytogenetic anomalies and teratogenic influences; it occurs as part of a syndrome, or due to heterozygous mutations in 1 of over 10 HPE-associated genes. ZIC2 mutations are the second-most common cause of non-syndromic non-chromosomal HPE (after sonic hedgehog) and occur de novo in 74% of the affected probands.

Objective: The objective of the study was to describe the first case of ZIC2-related HPE with both anterior and posterior pituitary insufficiencies.

Case Presentation: We report about a 2-year-8-month-old boy who was born as a second child in a non-consanguineous healthy Turkish family. He has the characteristic ZIC2 phenotype: bitemporal narrowing, upslanting palpebral fissures, large ears, short nose with anteverted nares and broad and deep philtrum. Magnetic resonance imaging revealed alobar HPE. During laboratory investigation, his blood sodium level was 158 mmol/L and the specific gravity of his urine was 1.002. Serum osmolarity was 336 mOsm/L and urine osmolality was 135 mOsm/kg. His FT4 was 0.8 ng/dL and TSH was 0.79 mLU/mL. Response to vasopressin confirmed the diagnosis of central diabetes insipidus and TRH-stimulating test supported the central hypothyroidism. A frameshift mutation (NM_007129.2:c1091_1092 del, p.Gln364Leufs*2) in the ZIC2 gene was detected.

Conclusion: Pituitary insufficiency other than isolated diabetes insipidus is a rare finding of HPE, and occurs most frequently in patients with GLI2 mutations (the phenotype of which typically does not include frank neuroanatomic anomalies such as HPE); ours is the only described patient with a ZIC2 mutation and both anterior and posterior pituitary dysfunction.
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http://dx.doi.org/10.1515/jpem-2013-0449DOI Listing
July 2014

Neuroprotective effects of farnesene against hydrogen peroxide-induced neurotoxicity in vitro.

Cell Mol Neurobiol 2014 Jan 9;34(1):101-11. Epub 2013 Oct 9.

Department of Molecular Biology and Genetics, Faculty of Science, Erzurum Technical University, Erzurum, Turkey,

Oxidative stress is highly damaging to cellular macromolecules and is also considered a main cause of the loss and impairment of neurons in several neurodegenerative disorders. Recent reports indicate that farnesene (FNS), an acyclic sesquiterpene, has antioxidant properties. However, little is known about the effects of FNS on oxidative stress-induced neurotoxicity. 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 different FNS isomers (α-FNS and β-FNS) and their mixture (Mix-FNS) in H2O2-induced toxicity in newborn rat cerebral cortex cell cultures for the first time. For this aim, both MTT and lactate dehydrogenase assays were carried out to evaluate cell viability. Total antioxidant capacity (TAC) and total oxidative stress (TOS) parameters were used to assess oxidative alterations. In addition to determining of 8-hydroxy-2-deoxyguanosine (8-OH-dG) levels in vitro, the comet assay was also performed for measuring the resistance of neuronal DNA to H2O2-induced challenge. Our results 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 (comet assay) increased in the group treated with H2O2 alone. But pretreatment of FNS suppressed the cytotoxicity, genotoxicity and oxidative stress, which were increased by H2O2 in clear type of isomers and applied concentration-dependent manners. The order of antioxidant effectiveness for modulating H2O2-induced oxidative stress-based neurotoxicity and genotoxicity is as β-FNS > Mix-FNS > α-FNS.
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http://dx.doi.org/10.1007/s10571-013-9991-yDOI Listing
January 2014

In vitro evaluation of long-term cytotoxic response of injection-molded polyamide and polymethyle metacrylate denture base materials on primary fibroblast cell culture.

Acta Odontol Scand 2013 Sep 3;71(5):1267-72. Epub 2013 Jul 3.

Department of Prosthetic Dentistry, Faculty of Dentistry, Inonu University, Malatya, Turkey.

Objective: This study investigated the long-term cytotoxic response of thermoplastic polyamide and conventional polymethyle metacrylate (PMMA) denture base materials.

Materials And Methods: Twenty discs were prepared for each polyamide, heat and cold cured PMMA denture base resins (totally 60) and divided into four sub-groups (n = 5). Cytotoxicity was assessed with the direct cell contact method using cell viability and neutral red (NR) uptake assay. Each sub-group was tested at initial and after being aged for 24 h, 1 week and 8 weeks with artificial saliva according to ISO 10993 standards.

Results: There were no significantly difference among the materials and control groups after initial, 24 h and 1 week testing. In 24 h testing, only Deflex was more toxic according to the Control group (p < 0.05). After 8 weeks of aging with artificial saliva, all materials were significantly cytotoxic when compared to the control group. QC20 was more toxic than Deflex and SC Cold Cure (p < 0.05). There were significant differences between the 8 week aging group and the initial, 24 h and 1 week testing for all materials (p < 0.05).

Conclusions: Cytotoxicity of all tested denture base materials increased significantly after the long-term aging. Therefore, long-term aging may be useful to determine a dental material's toxicity. Polyamide denture base material had a similar toxicity profile with conventional heat- and cold-cured PMMA.
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http://dx.doi.org/10.3109/00016357.2012.757648DOI Listing
September 2013

In vitro studies on chemoprotective effect of borax against aflatoxin B1-induced genetic damage in human lymphocytes.

Cytotechnology 2012 Dec 18;64(6):607-12. Epub 2012 Apr 18.

Department of Molecular Biology and Genetics, Faculty of Sciences, Erzurum Technical University, Erzurum, Turkey.

A common dietary contaminant, aflatoxin B1 (AFB1), has been shown to be a potent mutagen and carcinogen in humans and many animal species. Since the eradication of AFB1 contamination in agricultural products has been rare, the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. Boron compounds like borax (BX) and boric acid are the major components of industry and their antioxidant role has recently been reported. In the present report, we evaluated the capability of BX to inhibit the rate of micronucleus (MN) and sister chromatid exchange (SCE) formations induced by AFB1. There were significant increases (P < 0.05) in both SCE and MN frequencies of cultures treated with AFB1 (3.12 ppm) as compared to controls. However, co-application of BX (1, 2 and 5 ppm) and AFB1 resulted in decreases of SCE and MN rates as compared to the group treated with AFB1 alone. Borax gave 30-50 % protection against AFB1 induced SCEs and MNs. In conclusion, the support of borax was especially useful in aflatoxin-toxicated blood tissue. Thus, the risk on target tissues of AFB1 could be reduced and ensured early recovery from its toxicity.
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http://dx.doi.org/10.1007/s10616-012-9454-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488367PMC
December 2012

Borax counteracts genotoxicity of aluminum in rat liver.

Toxicol Ind Health 2013 Oct 4;29(9):775-9. Epub 2012 Apr 4.

1Department of Molecular Biology and Genetics, Erzurum Technical University, Erzurum, Turkey.

This study was carried out to evaluate the protective role of borax (BX) on genotoxicity induced by aluminum (Al) in rat liver, using liver micronucleus assay as an indicator of genotoxicity. Sprague-Dawley rats were randomly separated into six groups and each group had four animals. Aluminum chloride (AlCl₃; 5 mg/kg b.w.) and BX (3.25 and 13 mg/kg b.w.) were injected intraperitoneally to rats. Besides, animals were also treated with Al for 4 consecutive days followed by BX for 10 days. Rats were anesthetized after Al and BX injections and the hepatocytes were isolated for counting the number of micronucleated hepatocytes (MNHEPs). AlCl₃ was found to significantly (p < 0.05) increase the number of MNHEPs. Rats treated with BX, however, showed no increase in MNHEPs. Moreover, simultaneous treatments with BX significantly modulated the genotoxic effects of AlCl₃ in rats. It can be concluded that BX has beneficial influences and has the ability to antagonize Al toxicity.
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http://dx.doi.org/10.1177/0748233712442739DOI Listing
October 2013
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