請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6222
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 鄭景暉 | |
dc.contributor.author | Wen-Chih Shih | en |
dc.contributor.author | 施文智 | zh_TW |
dc.date.accessioned | 2021-05-16T16:23:28Z | - |
dc.date.available | 2013-09-24 | |
dc.date.available | 2021-05-16T16:23:28Z | - |
dc.date.copyright | 2013-09-24 | |
dc.date.issued | 2013 | |
dc.date.submitted | 2013-07-08 | |
dc.identifier.citation | Allen, E. P., S. C. Bayne, A. H. Brodine, R. J. Cronin, Jr., T. E. Donovan, J. C. Kois and J. B. Summitt (2001). 'Annual review of selected dental literature: report of the committee on scientific investigation of the American Academy of Restorative Dentistry.' J Prosthet Dent 86(1): 33-56.
Beckman, K. B. and B. N. Ames (1997). 'Oxidative decay of DNA.' J Biol Chem 272(32): 19633-19636. Bull, C. F., S. Beetstra-Hill, B. J. Benassi-Evans, J. W. Crott, M. Kimura, T. Teo, J. Wu and M. F. Fenech (2011). 'Application and adaptation of the in vitro micronucleus assay for the assessment of nutritional requirements of cells for DNA damage prevention.' Mutagenesis 26(1): 193-197. Caughman, G. B., G. S. Schuster and F. A. Rueggeberg (1999). 'Cell lipid alterations resulting from prolonged exposure to dimethylaminoethylmethacrylate.' Clin Oral Investig 3(4): 181-187. Cetinguc, A., S. Olmez and N. Vural (2007). 'HEMA diffusion from dentin bonding agents in young and old primary molars in vitro.' Dent Mater 23(3): 302-307. Chang, H. H., M. K. Guo, F. H. Kasten, M. C. Chang, G. F. Huang, Y. L. Wang, R. S. Wang and J. H. Jeng (2005). 'Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA.' Biomaterials 26(7): 745-753. Chang, M. C., Y. S. Ho, P. H. Lee, C. P. Chan, J. J. Lee, L. J. Hahn, Y. J. Wang and J. H. Jeng (2001). 'Areca nut extract and arecoline induced the cell cycle arrest but not apoptosis of cultured oral KB epithelial cells: association of glutathione, reactive oxygen species and mitochondrial membrane potential.' Carcinogenesis 22(9): 1527-1535. Chang, M. C., L. D. Lin, F. H. Chuang, C. P. Chan, T. M. Wang, J. J. Lee, P. Y. Jeng, W. Y. Tseng, H. J. Lin and J. H. Jeng (2012). 'Carboxylesterase expression in human dental pulp cells: role in regulation of BisGMA-induced prostanoid production and cytotoxicity.' Acta Biomater 8(3): 1380-1387. Cimpan, M. R., L. I. Cressey, N. Skaug, A. Halstensen, S. A. Lie, B. T. Gjertsen and R. Matre (2000). 'Patterns of cell death induced by eluates from denture base acrylic resins in U-937 human monoblastoid cells.' Eur J Oral Sci 108(1): 59-69. Cimpan, M. R., R. Matre, N. Skaug, S. A. Lie and H. Lygre (2005). 'The coinitiator DMABEE induces death by apoptosis and necrosis in human monoblastoid cells.' Clin Oral Investig 9(3): 168-172. Durner, J., U. I. Walther, J. Zaspel, R. Hickel and F. X. Reichl (2010). 'Metabolism of TEGDMA and HEMA in human cells.' Biomaterials 31(5): 818-823. Fadeel, B. and S. Orrenius (2005). 'Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease.' J Intern Med 258(6): 479-517. Fenech, M., M. Kirsch-Volders, A. T. Natarajan, J. Surralles, J. W. Crott, J. Parry, H. Norppa, D. A. Eastmond, J. D. Tucker and P. Thomas (2011). 'Molecular mechanisms of micronucleus, nucleoplasmic bridge and nuclear bud formation in mammalian and human cells.' Mutagenesis 26(1): 125-132. Fenech, M. and A. A. Morley (1986). 'Cytokinesis-block micronucleus method in human lymphocytes: effect of in vivo ageing and low dose X-irradiation.' Mutat Res 161(2): 193-198. Ferracane, J. L. (1994). 'Elution of leachable components from composites.' J Oral Rehabil 21(4): 441-452. Ferracane, J. L. and J. R. Condon (1990). 'Rate of elution of leachable components from composite.' Dent Mater 6(4): 282-287. Geurtsen, W., F. Lehmann, W. Spahl and G. Leyhausen (1998). 'Cytotoxicity of 35 dental resin composite monomers/additives in permanent 3T3 and three human primary fibroblast cultures.' J Biomed Mater Res 41(3): 474-480. Geurtsen, W., F. Lehmann, W. Spahl and G. Leyhausen (1998). 'Cytotoxicity of 35 dental resin composite monomers/additives in permanent 3T3 and three human primary fibroblast cultures.' Journal of Biomedical Materials Research 41(3): 474-480. Geurtsen, W., W. Spahl and G. Leyhausen (1998). 'Residual monomer/additive release and variability in cytotoxicity of light-curing glass-ionomer cements and compomers.' J Dent Res 77(12): 2012-2019. Guillen-Gosalbez, G. and A. Sorribas (2009). 'Identifying quantitative operation principles in metabolic pathways: a systematic method for searching feasible enzyme activity patterns leading to cellular adaptive responses.' BMC Bioinformatics 10: 386. Hofmann, N., J. Renner, B. Hugo and B. Klaiber (2002). 'Elution of leachable components from resin composites after plasma arc vs standard or soft-start halogen light irradiation.' J Dent 30(5-6): 223-232. Jazayeri, A., J. Falck, C. Lukas, J. Bartek, G. C. M. Smith, J. Lukas and S. P. Jackson (2006). 'ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks.' Nature Cell Biology 8(1): 37-U13. Kim, N. C., K. Ghanbari, D. A. Kracko, W. M. Weber, J. D. McDonald and K. J. Dix (2007). 'Identification of urinary metabolites of orally administered N,N-dimethyl-p-toluidine in male F344 rats.' Journal of Toxicology and Environmental Health-Part a-Current Issues 70(9-10): 781-788. Kodaka, T., M. Kobori, A. Hirayama and M. Abe (1999). 'Abrasion of human enamel by brushing with a commercial dentifrice containing hydroxyapatite crystals in vitro.' J Electron Microsc (Tokyo) 48(2): 167-172. Lapp, C. A. and G. S. Schuster (2002). 'Effects of DMAEMA and 4-methoxyphenol on gingival fibroblast growth, metabolism, and response to interleukin-1.' J Biomed Mater Res 60(1): 30-35. Lee, S., D. Pagoria, A. Raigrodski and W. Geurtsen (2007). 'Effects of combinations of ROS scavengers on oxidative DNA damage caused by visible-light-activated camphorquinone/N,N-Dimethyl-p-toluidine.' Journal of Biomedical Materials Research Part B-Applied Biomaterials 83B(2): 391-399. Lee, Y. J., H. N. Cho, D. I. Jeoung, J. W. Soh, C. K. Cho, S. Bae, H. Y. Chung, S. J. Lee and Y. S. Lee (2004). 'HSP25 overexpression attenuates oxidative stress-induced apoptosis: roles of ERK1/2 signaling and manganese superoxide dismutase.' Free Radic Biol Med 36(4): 429-444. Lepley, D. M., B. Li, D. F. Birt and J. C. Pelling (1996). 'The chemopreventive flavonoid apigenin induces G2/M arrest in keratinocytes.' Carcinogenesis 17(11): 2367-2375. Lygre, H., P. J. Hol, E. Solheim and G. Moe (1999). 'Organic leachables from polymer-based dental filling materials.' Eur J Oral Sci 107(5): 378-383. Lygre, H., M. Vorland and H. Holmsen (2001). 'Interaction of a dental filling material eluate and membrane lipids.' Clin Oral Investig 5(3): 167-171. Majno, G. and I. Joris (1995). 'Apoptosis, oncosis, and necrosis. An overview of cell death.' Am J Pathol 146(1): 3-15. Masgras, I., S. Carrera, P. J. de Verdier, P. Brennan, A. Majid, W. Makhtar, E. Tulchinsky, G. D. Jones, I. B. Roninson and S. Macip (2012). 'Reactive oxygen species and mitochondrial sensitivity to oxidative stress determine induction of cancer cell death by p21.' J Biol Chem 287(13): 9845-9854. Masuki, K., Y. Nomura, U. K. Bhawal, M. Sawajiri, I. Hirata, Y. Nahara and M. Okazaki (2007). 'Apoptotic and necrotic influence of dental resin polymerization initiators in human gingival fibroblast cultures.' Dental Materials Journal 26(6): 861-869. Mendiaz, E., M. Mamounas, J. Moffett and E. Englesberg (1986). 'A defined medium for and the effect of insulin on the growth, amino acid transport, and morphology of Chinese hamster ovary cells, CHO-K1 (CCL 61) and the isolation of insulin 'independent' mutants.' In Vitro Cell Dev Biol 22(2): 66-74. Moreau, M. F., D. Chappard, M. Lesourd, J. P. Montheard and M. F. Basle (1998). 'Free radicals and side products released during methylmethacrylate polymerization are cytotoxic for osteoblastic cells.' J Biomed Mater Res 40(1): 124-131. Murray, P. E., L. J. Windsor, A. A. Hafez, R. G. Stevenson and C. F. Cox (2003). 'Comparison of pulp responses to resin composites.' Oper Dent 28(3): 242-250. Nomura, Y., H. Ishibashi, M. Miyahara, R. Shinohara, F. Shiraishi and K. Arizono (2003). 'Effects of dental resin metabolites on estrogenic activity in vitro.' Journal of Materials Science-Materials in Medicine 14(4): 307-310. Nomura, Y., W. Teshima, T. Kawahara, N. Tanaka, H. Ishibashi, M. Okazaki and K. Arizono (2006). 'Genotoxicity of dental resin polymerization initiators in vitro.' Journal of Materials Science-Materials in Medicine 17(1): 29-32. Ortengren, U. (2000). 'On composite resin materials. Degradation, erosion and possible adverse effects in dentists.' Swed Dent J Suppl(141): 1-61. Pagoria, D., A. Lee and W. Geurtsen (2005). 'The effect of camphorquinone (CQ) and CQ-related photosensitizers on the generation of reactive oxygen species and the production of oxidative DNA damage.' Biomaterials 26(19): 4091-4099. Pashley, D. H. (1996). 'Dynamics of the pulpo-dentin complex.' Crit Rev Oral Biol Med 7(2): 104-133. Reichl, F. X., M. Esters, S. Simon, M. Seiss, K. Kehe, N. Kleinsasser, M. Folwaczny, J. Glas and R. Hickel (2006). 'Cell death effects of resin-based dental material compounds and mercurials in human gingival fibroblasts.' Arch Toxicol 80(6): 370-377. Roll, E. B., J. E. Dahl, G. Runningen and E. Morisbak (2004). 'In vitro cell death induced by irradiation and chemicals relevant for dental applications; dose-response and potentiation effects.' Eur J Oral Sci 112(3): 273-279. Samuelsen, J. T., J. E. Dahl, S. Karlsson, E. Morisbak and R. Becher (2007). 'Apoptosis induced by the monomers HEMA and TEGDMA involves formation of ROS and differential activation of the MAP-kinases p38, JNK and ERK.' Dent Mater 23(1): 34-39. Sanghani, S. P., P. C. Sanghani, M. A. Schiel and W. F. Bosron (2009). 'Human carboxylesterases: an update on CES1, CES2 and CES3.' Protein Pept Lett 16(10): 1207-1214. Savill, J., V. Fadok, P. Henson and C. Haslett (1993). 'Phagocyte recognition of cells undergoing apoptosis.' Immunol Today 14(3): 131-136. Schuster, G. S., J. F. Erbland, C. A. Lefebvre, G. B. Caughman and K. L. Knoernschild (1997). 'Effects of an aminomethacrylate on epithelial cell lipid metabolism.' J Biomater Sci Polym Ed 8(5): 363-375. Schweikl, H., A. Hartmann, K. A. Hiller, G. Spagnuolo, C. Bolay, G. Brockhoff and G. Schmalz (2007). 'Inhibition of TEGDMA and HEMA-induced genotoxicity and cell cycle arrest by N-acetylcysteine.' Dent Mater 23(6): 688-695. Schweikl, H., G. Spagnuolo and G. Schmalz (2006). 'Genetic and cellular toxicology of dental resin monomers.' Journal of Dental Research 85(10): 870-877. Schwengberg, S., H. Bohlen, N. Kleinsasser, K. Kehe, M. Seiss, U. I. Walther, R. Hickel and F. X. Reichl (2005). 'In vitro embryotoxicity assessment with dental restorative materials.' J Dent 33(1): 49-55. Seiss, M., C. Langer, R. Hickel and F. X. Reichl (2009). 'Quantitative determination of TEGDMA, BHT, and DMABEE in eluates from polymerized resin-based dental restorative materials by use of GC/MS.' Archives of Toxicology 83(12): 1109-1115. Seiss, M., W. Marquardt, R. Hickel and F. X. Reichl (2009). 'Excretion of dental resin monomers and metabolic intermediates via urine in guinea pigs.' Dent Mater 25(4): 481-485. Spagnuolo, G., V. D'Anto, C. Cosentino, G. Schmalz, H. Schweikl and S. Rengo (2006). 'Effect of N-acetyl-L-cysteine on ROS production and cell death caused by HEMA in human primary gingival fibroblasts.' Biomaterials 27(9): 1803-1809. Spahl, W., H. Budzikiewicz and W. Geurtsen (1998). 'Determination of leachable components from four commercial dental composites by gas and liquid chromatography/mass spectrometry.' J Dent 26(2): 137-145. Taira, M., H. Urabe, T. Hirose, K. Wakasa and M. Yamaki (1988). 'Analysis of photo-initiators in visible-light-cured dental composite resins.' J Dent Res 67(1): 24-28. Tjio, J. H. and T. T. Puck (1958). 'Genetics of somatic mammalian cells. II. Chromosomal constitution of cells in tissue culture.' J Exp Med 108(2): 259-268. Valko, M., D. Leibfritz, J. Moncol, M. T. Cronin, M. Mazur and J. Telser (2007). 'Free radicals and antioxidants in normal physiological functions and human disease.' Int J Biochem Cell Biol 39(1): 44-84. Vral, A., M. Fenech and H. Thierens (2011). 'The micronucleus assay as a biological dosimeter of in vivo ionising radiation exposure.' Mutagenesis 26(1): 11-17. Winter, K., D. Pagoria and W. Geurtsen (2005). 'The effect of antioxidants on oxidative DNA damage induced by visible-light-irradiated camphorquinone/N,N-dimethyl-p-toluidine.' Biomaterials 26(26): 5321-5329. Yap, A. U., V. T. Han, M. S. Soh and K. S. Siow (2004). 'Elution of leachable components from composites after LED and halogen light irradiation.' Oper Dent 29(4): 448-453. Jayapal K. P., Wlaschin K. F., Yap M. G. S., Hu W-S., (2007). 'Recombinant protein therapeutics from CHO cells — 20 years and counting.'. Chem. Eng. Prog. 103(10): 40–47. Cooper GM (2000). 'Chapter 14: The Eukaryotic Cell Cycle'. The cell: a molecular approach (2nd ed.). Washington, D.C: ASM Press. ISBN 0-87893-106-6. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6222 | - |
dc.description.abstract | Resin-containing products are widely applied in modern dentistry. Chemical substances released from the materials may cause cytotoxicity and adverse biological effects. N,N-Dimethyl-p-toluidine (DMPT), 2-Dimethylaminoethyl methacrylate (DMAEMA) and 4-Dimethylaminobenzoic acid ethyl ester (DMABEE) are three chemicals released from composite resins. Because of moderate toxicity, they were less investigated in previous studies. However, these three chemicals do not bond to composite resin after curing and are released to oral cavities for a long time. Thus, it is necessary to examine their cytoxicity and toxic mechanism. Investigations of cell growth, cell cycle progression, reactive oxygen species (ROS) production and DNA damage are valuable direction to realize the mechanism, thus were applied in the present studies to get insight into the chemicals-induced toxicity.
First of all, we evaluated the effect of DMPT on CHO-K1 cells. DMPT induced both short-term and long-term growth inhibition of CHO-K1 cells. In the mean time, the ratio of micronuclei (MNi) increased in a dose-dependent manner. However, ROS production was not elevated and N-acetyl-cysteine (NAC) could not rehabilitate the growth potential. On cell cycle analysis, after treating with DMPT, there were no obvious arrest at different phases of cell cycle compared to control group. Moreover, the mode of cell death most accumulated in necrosis. According to the results from above, it suggested that ROS production was not the main cause of CHO-K1 cell death and we needed to examine other pathways to explain of DNA damage and cell death. DMAEMA also produced growth inhibition of CHO-K1 cells in the same pattern compared to DMPT. But, the effect of DNA damage of DMAEMA was weaker than DMPT. Only under 3.5 mM DMAEMA, the amount of MNi rised slightly. Similarly, ROS production obviously increased when CHO-K1 cells exposed to the highest concentration DMAEMA. However, we found that the cell cycle arrested at S and Sub-G0/G1 phase started from 1.5 mM DMAEMA. This result implied that the cells might get into apoptosis. Thus, first, we could state that DMAEMA could induce CHO-K1 cells death by ROS production, but the ability of self-repairing might alleviate the toxicity of DMAEMA. Secondary, due to different results of DNA damage between DMPT and DMAEMA, we hypothesize that they induced cell death by different mechanism. Among three drugs, DMABEE was the most toxic to CHO-K1 cells. It elicited growth inhibition of CHO-K1 cells in a dose-dependent manner, and at a much lower concentration compared to DMPT and DMAEMA. In short-term inhibition, 0.75 mM DMABEE induced about 50% down-regulation of growth capacity; in long-term inhibition, there were obvious decrease of growth potential from 0.25 mM DMABEE. Further, in morphology, CHO-K1 cells changed from cuboid- or round-shape to fibroblastic variation under high concentrations of DMABEE. However, the morphologic change could be recovered by pre-treating with carboxylesterases (CES). Similarly, after co-incubating with CES, the growth inhibition of CHO-K1 cells by DMABEE could be prevented. In CBMN assays, the percentage of MNi elevated started from 0.25 mM DMABEE. The cells were severely broken and could not be calculated by treating with 1.0 mM DMABEE. ROS production of CHO-K1 cells also increased in a dose-related manner of DMABEE. But, there was no prevention of growth inhibition after pre-incubating with NAC. We believed that NAC played a role of pro-oxidant instead of anti-oxidant. Thus, the growth inhibition of CHO-K1 cells dramatically increased. The cell cycle got arrested on G0/G1 phase started from treating with 0.25 mM DMABEE and the cell residing in the quadrant of necrosis and late apoptosis would increase. Theses results indicated that CHO-K1 cells would death through DNA damage by ROS attack and cause cell necrosis or late apoptosis. The present studies helped us to elucidate the cytotoxic mechanism of these three chemicals leached from composite resins. Although the cytotoxic concentration reported by us might not reached in prudent application. while lacking sufficient thickness of dentin or poor polymerization, the unbound chemical substances could lead potential toxic effect to the pulp tissue. | en |
dc.description.provenance | Made available in DSpace on 2021-05-16T16:23:28Z (GMT). No. of bitstreams: 1 ntu-102-R99422009-1.pdf: 12831063 bytes, checksum: 389a095c66d1fa6424f4aed39e105452 (MD5) Previous issue date: 2013 | en |
dc.description.tableofcontents | 中文摘要...........................................................................................................................i
Abstract...........................................................................................................................iii Chapter I Literature Review...........................................................................................1 1.1 Introduction...........................................................................................................1 1.2 Chemicals (or components) leached out from composite resins...........................2 1.3 N,N-Dimethyl-p-toluidine (DMPT)......................................................................3 1.4 2-Dimethylaminoethyl methacrylate (DMAEMA)...............................................5 1.5 4-Dimethylaminobenzoic acid ethyl ester (DMABEE).........................................6 1.6 Chinese hamster ovary (CHO) cells and CHO-K1 cells.......................................8 1.7 Apoptosis and necrosis..........................................................................................8 1.8 Reactive oxygen species (ROS)............................................................................9 1.9 Cell cycle.............................................................................................................11 1.10 DNA damage.....................................................................................................12 1. 11 Carboxylesterase (CES) in resin metabolism...................................................14 Chapter II The purpose and hypothesis of the study.................................................16 Chapter III Materials & Methods................................................................................17 3.1 Chemicals............................................................................................................17 3.2 CHO-K1 cells and cell culture.............................................................................18 3.3 Evaluation of cell growth....................................................................................18 3.4 ROS detection (DCF flow cytometry)/GSH depletion (CMF flow cytometry)..19 3.5 Apoptosis and necrosis (PI & Annexin V flow cytometry).................................20 3.6 Cell cycle (PI flow cytometry)............................................................................21 3.7 DNA damage (CBMN assay with IF)..................................................................21 3.8 Statistical analysis................................................................................................22 Chapter IV Results........................................................................................................23 4.1 Effects of DMPT, DMAEMA and DMABEE on CHO-K1 cells........................23 4.1.1 Growth assay...............................................................................................23 4.1.2 Morphological alteration of CHO-K1 cells................................................24 4.1.3 Annexin V-FITC / PI assay.........................................................................25 4.1.4 PI assay.......................................................................................................26 4.1.5 DCF assay & CMF assay............................................................................27 4.1.6 CBMN assay with IF stain..........................................................................29 4.2 Effects of NAC, catalase, & carboxylesterase on DMPT-, DMAEMA- or DMABEE-induced cell growth inhibition..................................................................30 4.2.1 Effect of NAC, catalase and carboxylesterase on CHO-K1 cells................30 Chapter V Discussion....................................................................................................32 5.1 Morphological and proliferation aberrations..........................................................32 5.2 Cell death induction................................................................................................33 5.3 Effect on cell cycle.................................................................................................34 5.4 ROS induction........................................................................................................35 5.5 GSH depletion........................................................................................................36 5.6 DNA damage..........................................................................................................37 5.7 Inhibitors & enzymes..............................................................................................39 5.8 Clinical consideration.............................................................................................40 Chapter VI Conclusion..................................................................................................42 Reference........................................................................................................................44 Figures Fig. 1.1a & b Effect of DMPT on the growth of CHO-K1 cells.....................................................52 Fig. 1.2a & b Effect of DMAEMA on the growth of CHO-K1 cells..............................................53 Fig. 1.3a & b Effect of DMABEE on the growth of CHO-K1 cells...............................................54 Fig. 2.1a & b Morphology alternation of CHO-K1 cells (DMPT)...................................................55 Fig. 2.2a & b Morphology alternation of CHO-K1 cells.. (DMAEMA)..........................................55 Fig. 2.2a & b Morphology alternation of CHO-K1 cells.. (DMABEE)...........................................56 Fig. 2.4a & b Morphology alternation of CHO-K1 cells via immunofluorescence staining..........56 Induction of necrosis and apoptosis of CHO-K1 cells by DMABEE................................................57 Fig. 3.1a, b & c Effect of three chemicals analysis by Annexin V-FITC / PI assay flow cytometry............................................................................................................................................58 Effects of DMSO on the cell cycle progression (G0/G1;S;G2/M phase)..................................................................................................................................................59 Effects of DMSO on the cell cycle progression (Sub-G0/G1 phase)................................................59 Fig. 4.1a, b & c Effect of three chemicals on the cell cycle of CHO-K1 cells (G0/G1, S, G2/M).......................................................................................................................................................60 Fig. 4.2a, b & c Effect of three chemicals on the cell cycle of CHO-K1 cells (Sub-G0/G1)..........61 Effects of DMPT on the DCF expression of CHO-K1 cells.............................................................62 Fig. 5.1a, b & c Effect of three chemicals analysis by DCF flow cytometry..................................63 Effects of DMPT on the CMF expression of CHO-K1 cells.............................................................64 Fig. 5.2a, b & c Effect of three chemicals analysis by CMF flow cytometry..................................65 Fig. 6.1a & b CBMN assay of CHO-K1 cells (DMPT)..................................................................66 Fig. 6.2a & b CBMN assay of CHO-K1 cells (DMAEMA)...........................................................67 Fig. 6.3a & b CBMN assay of CHO-K1 cells (DMABEE).............................................................68 Fig. 7.1a & b Effect of CHO-K1 cells co-treating with NAC on the growth ability.......................69 Fig. 7.2a & b Effect of CHO-K1 cells co-treating with catalase on the growth ability...................70 Fig. 7.3a, b & c Effect of CHO-K1 cells co-treating with carboxylesterase on the growth ability..................................................................................................................................................71 | |
dc.language.iso | en | |
dc.title | 三種牙科樹脂之化學成分毒性效應之分析 | zh_TW |
dc.title | Investigation of Toxic Effects of Three Dental Resin Chemicals | en |
dc.type | Thesis | |
dc.date.schoolyear | 101-2 | |
dc.description.degree | 碩士 | |
dc.contributor.coadvisor | 張曉華 | |
dc.contributor.oralexamcommittee | 黃翠賢,張美姬,陳羿貞 | |
dc.subject.keyword | DMPT,DMAEMA,DMABEE,細胞毒性,細胞週期,ROS,DNA damage
, | zh_TW |
dc.subject.keyword | DMPT,DMAEMA,DMABEE,cytotoxicity,cell cycle,ROS,DNA damage, | en |
dc.relation.page | 71 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2013-07-08 | |
dc.contributor.author-college | 牙醫專業學院 | zh_TW |
dc.contributor.author-dept | 臨床牙醫學研究所 | zh_TW |
顯示於系所單位: | 臨床牙醫學研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-102-1.pdf | 12.53 MB | Adobe PDF | 檢視/開啟 |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。