Cytotoxicity of Three Light-Cured Orthodontic Adhesives

2018 ◽  
Vol 777 ◽  
pp. 582-586 ◽  
Author(s):  
Natthasit Pudpong ◽  
Niwat Anuwongnukroh ◽  
Surachai Dechkunakorn ◽  
Wassana Wichai ◽  
Peerapong Tua-Ngam

Objective: The aim of this study was to evaluate the cytotoxic effects of three commercial light-cured orthodontic adhesives.Materials and methods: The potential cytotoxic effects of three types of orthodontic adhesives, Grengloo, Green Glue, and Transbond XT, were tested on L929 cell culture. The cell line was grown in 96-well tissue culture plates (1x105 cells/mm3). Thin resin discs weighing 0.4, 0.6, 0.8, 0.8, and 0.8 gram of each material were prepared and aged for 1, 3, 6, 8, and 10 days, respectively, in Minimum Essential Medium (MEM) at 37°C with 5% CO2 at 100% humidity. Cell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay according to ISO 10993-5: 2009 (E). The differences among the groups was statically analyzed by independent paired t-test (α = 0.05).Results: After 1 day of storage, all adhesive systems showed cytotoxic effects. However, ageing tended to considerably reduce the cytotoxicity of Green Glue. Grengloo was essentially non-cytotoxic day 3 onwards, while Green Glue and Transbond XT exhibited potential cytotoxicity at all times of the experiment. Conclusion: All tested light-cured orthodontic adhesives had cytotoxic potential during the first day. Grengloo had the highest cell viability, whereas, Green Glue had the lowest.

2019 ◽  
Vol 294 ◽  
pp. 65-70
Author(s):  
Kanin Nimcharoensuk ◽  
Niwat Anuwongnukroh ◽  
Surachai Dechkunakorn ◽  
Vanthana Sattabanasuk ◽  
Panya Sunintaboon ◽  
...  

The objective of this study was to compare the cytotoxicity of a domestically-made light-cured orthodontic adhesive to a commercial adhesive, Transbond XT (3M Unitek, USA). An in-house orthodontic adhesive composed of a filler 60-70 weight % and a monomer ratio (BisGMA:TEGDMA) of 6:4 with 0.5% of photoinitiator was mixed. The potential cytotoxic effect of this experimental and a control adhesive was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay according to ISO 10993-5: 2009(E). The L929 cell line was grown in 96-well tissue culture plates (1x105 cells/mm3). Thin cured-resin discs of each material weighing 0.4 gram were prepared and incubated for 1, 3, 5, 7, 14, and 30 days in Dulbecco’s modified Eagle medium (DMEM) at 37°C and 95% humidity with 5% CO2. The percentage of cell viability was reported by descriptive statistics. The result showed that the cell viability of the experimental adhesive was higher than Transbond XT in all measured periods. The cytotoxicity of both the adhesives gradually decreased with the progression of time. In conclusion, the in-house adhesive showed a good biocompatibility since the first day following polymerization. On the other hand, Transbond XT started with a cytotoxic potential, then, turned to be non-cytotoxic after 5 days of curing.


2014 ◽  
Vol 33 (10) ◽  
pp. 1000-1007 ◽  
Author(s):  
B Çörekçi ◽  
C Irgın ◽  
K Halıcıoğlu ◽  
S Dursun ◽  
MZ Yavuz

Objectives: The aim of this study was to evaluate, the cytotoxicity of orthodontic composites in vitro as a function of degree of conversion (DC) and the light curing units (LCU) employed on mouse fibroblast (L929). Materials and Methods: Cured samples of the composites Light bond ( Reliance Orthodontic Products, Itasca, Illinois, USA), Ortho bracket paste (Bisco, Schaumburg, Illinois, USA), Opal bond MV (OPAL, South Jordan, Utah, USA), and Transbond XT (3M, Monrovia, California, USA) were prepared. Polymerization was performed with two LCUs: VALO Ortho (Ultradent, South Jordan, Utah, USA) is a third-generation LCU and Elipar S10 (3M, USA) is a second-generation LCU. Four samples were immersed in cell culture medium to obtain composite extracts. After incubation of L929 cell cultures with the extracts obtained, cytotoxicity was determined using the methyl tetrazolium test. Fourier transform infrared spectroscopy (FTIR) was used to evaluate DC for five samples. A multivariate analysis of variance (ANOVA), two-way ANOVA, and Tukey’s honestly significant difference test were utilized for statistical analyses. Results: Cytotoxicity and DC of all tested composites ( p < 0.001) and the interaction between composites and LCUs ( p < 0.01) were significantly different. LCUs had no significant influence on the cytotoxicity and DC of composite materials ( p > 0.05). The correlations between cell viability and DC were positive for three composites but statistically insignificant. Conclusion: Composites and LCUs must be matched with one another to result in satisfactory maximal biocompatibility and DC. Opal Bond plasma light-emitting diode combination was a better choice for cell viability. Three composites showed a positive correlation between cytotoxicity and DC. Therefore high-intensity LCUs can be said to efficiently affect polymerization, and so, higher DC rates may achieve higher cell viability rates.


2007 ◽  
Vol 86 (5) ◽  
pp. 441-445 ◽  
Author(s):  
M.T. Costa ◽  
M.A. Lenza ◽  
C.S. Gosch ◽  
I. Costa ◽  
F. Ribeiro-Dias

The corrosion resistance of AISI 304 stainless steel (AISI 304 SS) and manganese stainless steel (low-nickel SS) brackets in artificial saliva was investigated. The cytotoxic effects of their corrosion products on L929 cell culture were compared by two assays, crystal violet, to evaluate cell viability, and MTT (3-[4,5-dimethylthiazol-2-yl]2,5-diphenyltetrazolium bromide), for cell metabolism and proliferation. The atomic absorption spectroscopic analysis of the corrosion products demonstrated that nickel and manganese ion concentrations were higher for the AISI 304 SS-bracket immersion solution as compared with the low-nickel SS brackets. Scanning electron microscopy and energy-dispersive spectroscopy demonstrated less corrosion resistance for the AISI 304 SS brackets. Although none of the bracket extracts altered L929 cell viability or morphology, the AISI 304 SS-bracket extracts decreased cellular metabolism slightly. The results indicated that the low-nickel SS presents better in vitro biocompatibility than AISI 304 SS brackets. Abbreviations used: AISI, American Iron and Steel Institute; EDS, energy-dispersive spectroscopy; OD, optical density; ISO, International Organization for Standardization; MTT, (3-{4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NiSO4, nickel sulfate; SEM, standard error of the mean; WHO, World Health Organization; and TNF, tumor necrosis factor.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Mohammad Mazloum-Ardakani ◽  
Behnaz Barazesh ◽  
Seyed Mohammad Moshtaghioun ◽  
Mohammad Hasan Sheikhha

Abstract For the first time ever, this paper reports the development of an easily operated and cost-effective electrochemical assay to be used as an appropriate substitute for the MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) cell viability assay. The proposed assay is based on the electrochemical reaction of Saccharomyces cerevisiae (S. cerevisiae) with toxic materials, and it overcomes most of the limitations of MTT such as evaporation of volatile solvents, cytotoxic effects of MTT reagents, high cost, and sensitivity to light. The novel electrochemical assay can be used to detect diazinon in the range of 10−6 g mL−1 to 10−2 g mL−1 with the detection limit of 1.5 × 10−7 g mL−1.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Vincenza Cannella ◽  
Roberta Altomare ◽  
Gabriele Chiaramonte ◽  
Santina Di Bella ◽  
Francesco Mira ◽  
...  

Objective. The aim of this study was to evaluate the cytotoxic potential of a type of endodontic pin on L929 cell line according to the UNI EN ISO 10993/2009 rule. Methods. L929 cells were used for the assays; extracts were prepared from three different-diameter endodontic pins, made of epoxy resin and fiberglass matrix and from Reference Materials (ZDEC, ZDBC, and HDP films). MTS assay was performed after 24 h, 48 h, and 72 h of exposure of L929 cells to pin and Reference Material extracts, 5% phenol solution, and control reagent. Cells cultured with different media containing extracts were monitored for up to 72 h and stained with haematoxylin/eosin. Results. Pins of different diameters had no cytotoxic effects on L929 cells at 24 h, 48 h, and 72 h (all values >70%). Cells cultured in medium containing pin extracts grew without any differences compared to the control cells. Conclusion. The endodontic pins tested showed no cytotoxic effects and did not induce changes in morphology for up to 72 h.


Author(s):  
Amber M. Tavener ◽  
Megan C. Phelps ◽  
Richard L. Daniels

AbstractGlioblastoma (GBM) is a lethal astrocyte-derived tumor that is currently treated with a multi-modal approach of surgical resection, radiotherapy, and temozolomide-based chemotherapy. Alternatives to current therapies are urgently needed as its prognosis remains poor. Anthracyclines are a class of compounds that show great potential as GBM chemotherapeutic agents and are widely used to treat solid tumors outside the central nervous system. Here we investigate the cytotoxic effects of doxorubicin and other anthracyclines on GL261 glioma tumor cells in anticipation of novel anthracycline-based CNS therapies. Three methods were used to quantify dose-dependent effects of anthracyclines on adherent GL261 tumor cells, a murine cell-based model of GBM. MTT assays quantified anthracycline effects on cell viability, comet assays examined doxorubicin genotoxicity, and flow cytometry with Annexin V/PI staining characterized doxorubicin-induced apoptosis and necrosis. Dose-dependent reductions in GL261 cell viability were found in cells treated with doxorubicin (EC50 = 4.9 μM), epirubicin (EC50 = 5.9 μM), and idarubicin (EC50 = 4.4 μM). Comet assays showed DNA damage following doxorubicin treatments, peaking at concentrations of 1.0 μM and declining after 25 μM. Lastly, flow cytometric analysis of doxorubicin-treated cells showed dose-dependent induction of apoptosis (EC50 = 5.2 μM). Together, these results characterized the cytotoxic effects of anthracyclines on GL261 glioma cells. We found dose-dependent apoptotic induction; however at high concentrations we find that cell death is likely necrotic. Our results support the continued exploration of anthracyclines as compounds with significant potential for improved GBM treatments.


OTO Open ◽  
2021 ◽  
Vol 5 (2) ◽  
pp. 2473974X2110092
Author(s):  
Jivianne T. Lee ◽  
Saroj Basak

Although the etiology of chronic rhinosinusitis remains unknown, environmental factors including airborne pollutants and toxicants are postulated to contribute to its pathogenesis. However, the precise pathomechanisms with which environmental toxicants may contribute to chronic rhinosinusitis are not fully understood. The purpose of this pilot study is to examine the cytotoxic effects of N,N-diethyl- meta-toluamide (DEET), a commonly used pesticide, on sinonasal epithelial cells (SNECs). Sinus mucosa was obtained from 3 subjects without a history of chronic rhinosinusitis. Cultured SNECs were exposed to various concentrations of DEET (0-5 mM) for 6 days. Cell viability, proliferation, and morphologic changes were assessed using the MTT colorimetric dye assay and the Incucyte Live Cell Monitoring System. Statistically significant dose-dependent reduction in cell viability and proliferation was observed between exposure and control groups ( P < .05) at all concentrations tested. Dose-dependent cellular morphological changes were also seen. These findings indicate that DEET exposure induces dose-dependent cytotoxicity in sinonasal epithelia.


Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769756 ◽  
Author(s):  
Jia-Teng Zhong ◽  
Jian Yu ◽  
Hai-Jun Wang ◽  
Yu Shi ◽  
Tie-Suo Zhao ◽  
...  

Nowadays, although chemotherapy is an established therapy for breast cancer, the molecular mechanisms of chemotherapy resistance in breast cancer remain poorly understood. This study aims to explore the effects of endoplasmic reticulum stress on autophagy, apoptosis, and chemotherapy resistance in human breast cancer cells by regulating PI3K/AKT/mTOR signaling pathway. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed to detect the cell viability of six human breast cancer cell lines (MCF-7, ZR-75-30, T47D, MDA-MB-435s, MDA-MB-453, and MDA-MB-231) treated with tunicamycin (5 µM), after which MCF-7 cells were selected for further experiment. Then, MCF-7 cells were divided into the control (without any treatment), tunicamycin (8 µ), BEZ235 (5 µ), and tunicamycin + BEZ235 groups. Cell viability of each group was testified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Western blotting was applied to determine the expressions of endoplasmic reticulum stress and PI3K/AKT/mTOR pathway–related proteins and autophagy- and apoptosis-related proteins. Monodansylcadaverine and Annexin V–fluorescein isothiocyanate/propidium iodide staining were used for determination of cell autophagy and apoptosis. Furthermore, MCF-7 cells were divided into the control (without any treatment), tunicamycin (5 µM), cisplatin (16 µM), cisplatin (16 µM) + BEZ235 (5 µM), tunicamycin (5 µM) + cisplatin (16 µM), and tunicamycin (5 µM) + cisplatin (16 µM) + BEZ235 groups. Cell viability and apoptosis were also evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Annexin V–fluorescein isothiocyanate/propidium iodide staining. In MCF-7 cells treated with tunicamycin, cell viability decreased significantly, but PEAK, eIF2, and CHOP were upregulated markedly and p-PI3K, p-AKT, and p-MTOR were downregulated in dose- and time-dependent manners. In the tunicamycin + BEZ235 group, the cell viability was lower and the apoptosis rate was higher than those of the control and monotherapy groups. Compared with the cisplatin group, the tunicamycin + cisplatin group showed a relatively higher growth inhibition rate; the growth inhibition rate substantially increased in the tunicamycin + cisplatin + BEZ235 group than the tunicamycin + cisplatin group. The apoptosis rate was highest in tunicamycin + cisplatin + BEZ235 group, followed by tunicamycin + cisplatin group and then cisplatin group. Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway.


2014 ◽  
Vol 34 (8) ◽  
pp. 848-855 ◽  
Author(s):  
I Hwang ◽  
JW Lee ◽  
JS Kim ◽  
HW Gil ◽  
HY Song ◽  
...  

Objective: Self-poisoning with (4-chloro-2-methylphenoxy) acetic acid (MCPA) is a common reason for presentation to hospitals, especially in some Asian countries. We encountered a case of a 76-year-old woman who experienced unconsciousness, shock and respiratory failure after ingesting 100 mL MCPA herbicide. We determined whether the surfactant in the formulation was the chemical responsible for the toxic symptom in this patient. Design: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell viability and lactate dehydrogenase (LDH) cytotoxicity assays were performed on human brain neuroblastoma SK-N-SH cells. The expressions of 84 genes in 9 categories that are implicated in cellular damage pathways were quantified using an RT2 Profiler™ PCR array on a human neuronal cell line challenged with polyoxyethylene tridecyl ether (PTE). Setting: Pesticide intoxication institute in university hospital. Interventions: Extracorporeal elimination with intravenous lipid emulsion. Measurements: Cell viability and gene expression. Main Results: In the MTT assay, MCPA only minimally decreased cell viability even at concentrations as high as 1 mM. Cells treated with 1-methoxy-2-propanol, dimethylamine and polypropylene glycol exhibited minimal decreases in viability, whilst the viability of cells challenged with PTE decreased dramatically; only 15.5% of cells survived after exposure to 1 µM PTE. Similarly, the results of the LDH cytotoxicity assay showed that MCPA had very low cytotoxicity, whilst cells treated with PTE showed incomparably higher LDH levels ( p < 0.0001). PTE up-regulated the expressions of genes implicated in various cell damage pathways, particularly genes involved in the inflammatory pathway. Conclusions: The surfactant PTE was likely the chemical responsible for the toxic symptom in our patient.


Author(s):  
Pei-Tzu Li ◽  
Ying-Chu Lee ◽  
Namasivayam Elangovan ◽  
Sin-Tak Chu
Keyword(s):  

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