Cyto- i genotoksyczność wybranych składników materiałów kompozycyjnych i ich systemów wiążących



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Podsumowanie


Materiały dentystyczne tworzone na bazie żywic metakrylanowych są powszechnie stosowane w stomatologii. Jedną z wad tego rodzaju wypełnień jest uwalnianie się z nich różnych substancji m.in. monomerów metakrylanowych. Ponieważ pacjenci posiadający wypełnienia na bazie żywic są narażeni na uwalniające się z nich monomery przez długi okres czasu, a często przez całe życie, ważne jest badanie wpływu tych związków na organizm człowieka.

Wyniki dotychczas przeprowadzonych badań wskazują na cyto- i genotoksyczne działanie związków metakrylanowych. HEMA i TEGDMA zaburzają prawidłową strukturę komórki np. poprzez oddziaływanie z błoną komórkową, jak również jej funkcjonowanie np. zmniejszając poziom glutationu w komórce, który jest odpowiedzialny za ochronę struktur komórki i detoksyfikację. Monomery metakrylanowe zwiększają poziom wolnych rodników tlenowych, co prowadzi do zakłócenia wewnątrzkomórkowej równowagi redoks. Stres oksydacyjny będący wynikiem zachwianej równowagi pomiędzy wewnątrzkomórkowymi antyoksydantami


i oksydantami prowadzi do zatrzymania cyklu komórkowego czy indukcji apoptozy. Ponadto HEMA i TEGDMA zmieniają poziom ekspresji wielu genów ważnych dla procesów proliferacji, kontroli cyklu komórkowego i śmierci komórki oraz dla replikacji i naprawy DNA. Związki te oddziałują również na mediatory reakcji zapalnej, takie jak interleukina-6, co może spowodować spowolnienie gojenia się ran czy wywoływać stany zapalne tkanek np. przyzębia.

Nie tylko monomery są toksyczne dla organizmu człowieka, równie ważne jest określenie wpływu produktów ich metabolizmu na strukturę i funkcje komórki. Wykazano, że monomery mogą być degradowane do toksycznych epoksydów powstających z kwasu metakrylanowego, który jest produktem pośrednim. Aby w pełni poznać mechanizmy odpowiedzialne za cyto- i genotoksyczność spowodowaną związkami metakrylanowymi potrzebne są dalsze badania. Większość doświadczeń mających na celu zbadanie efektu działania TEGDMA i HEMA była przeprowadzona in vitro. W celu weryfikacji uzyskanych do tej pory wyników niezbędne jest przeprowadzenie analogicznych badań in vivo, z użyciem modelowych organizmów. Równie istotne jest zbadanie wpływu monomerów metakrylanowych na komórki krwi obwodowej, gdyż związki te są uwalniane z wypełnień do okolicznych tkanek,


a następnie do krwiobiegu. Niekompletna polimeryzacja prowadząca do uwalniania się różnych substancji oraz obkurczanie popolimeryzacyjne skutkujące rozwojem wtórnej próchnicy to główne problemy związane z metakrylanowymi materiałami dentystycznymi. Niezwykle ważne wydaje się więc prowadzenie badań w kierunku modyfikacji aktualnie stosowanych wypełnień na bazie żywic. Modyfikacje mogą prowadzić do zwiększenia stopnia konwersji monomerów w polimer czy zminimalizowania zjawiska obkurczania się materiału wypełniającego. Ponadto powinny być prowadzone poszukiwania substancji, która w połączeniu z żywicami metakrylanowymi chroniłaby strukturę polimeru przed degradacją.

Dogłębna wiedza dotycząca mechanizmów odpowiedzialnych za toksyczność monomerów metakrylanowych może pomóc w zrozumieniu ich wpływu na organizm człowieka, a badania nad udoskonaleniem właściwości fizycznych i chemicznych tych związków mogą sprzyjać ochronie ludzkiego zdrowia.


Piśmiennictwo

1. About I, Camps J, Mitsiadis TA, Bottero MJ, Butler W, Franquin JC: Influence of resinous monomers on the differentiation in vitro of human pulp cells into odotoblasts. J Biomed Mater Res 2002, 63: 418-423.

2. Asp J, Thornemo M, Inert S, Lindahl A: The helix-loop-helix transcription factors Id1 and Id3 have a functional role in control of cell division in human normal and neoplastic chondrocytes. FEBS Lett 1998, 438: 85-90.

3. Baeuerle PA, Henkel T: Function and activation of NF-kappaB in the immune system. Annu Rev Immunol 1994, 12: 141-179.

4. Bean TA, Zhuang WC, Tong PY, Eick JD, Yourtee DM: Effect of esterase on methacrylates and methacrylate polymers in an enzyme simulator for biodurability and biocompatibility testing. J Biomed Mater Res 1994, 28: 59-63.

5. Beg AA, Baltimore D: An essential role for NF-kappaB in preventing TNF alpha-induced cell death. Science 1996, 274: 782-784.

6. Bouillaguet S, Wataha JC, Hanks CT, Ciucchi B, Holz J: In vitro cytotoxicity and dentin permeability of HEMA. J Endod 1996, 22: 244-248.

7. Chang HH, Guo MK, Kasten FH, Chang MC, Huang GF, Wang YL, Wang RS, Jeng JH: Stimulation of glutathione depletion, ROS production and cell cycle arrest of dental pulp cells and gingival epithelial cells by HEMA. Biomaterials 2005, 26: 745-753.

8. Cook WD: Polymerization defects in composite resins. Red. Smith DC w: Posterior composite resin dental restorative materials. Peter Szulc Publishing Co., Holandia 1985, str. 273-286.

9. Corcoran CA, Luo X, He Q, Jiang C, Huang Y, Sheikh MS: Genotoxic and endoplasmic reticulum stresses differentially regulate TRB3 expression. Cancer Biol Ther 2005, 4: 1063-1067.

10. Davidson CL, Feilzer AJ: Polymerization shrinkage and polymerization shrinkage stress in polymer–based restoratives. J. Dent 1997, 25: 435-440.

11. De Munck J, Van Landuyt K, Peumans M, Poitevin A, Lambrecht P, Braem M, Van Meerbek B: A critical review of the durability of adhesion to tooth tissue: methods and results. J Dent Res 2005, 84: 118–132.

12. Eckerdt F, Yuan J, Strebhardt K: Polo-like kinases and oncogenesis. Oncogene 2005, 24: 267-276.

13. Ellisen LW, Ramsayer KD, Johannessen CM, Yang A, Beppu H, Minda K, Oliner JD, McKeon F, Haber DA: REDD1, a developmentally regulated transcriptional target of p63 and p53, links p63 to regulation of reactive oxygen species. Mol Cell 2002, 10: 995-1005.

14. Emmler J, Seiss M, Kreppel H, Reichl FX, Hickel R, Kehe K: Cytotoxicity of the dental composite component TEGDMA and selected metabolic by-products in human pulmonary cells. Dent Mater 2008, vol.24, 12: 1670-1675.

15. Engelmann J, Leyhausen G, Leibfritz D, Geurtsen W: Metabolic effects of dental resin components in vitro detected by NMR spectroscopy. J Dent Res 2001, 80: 869-875.

16. Engelmann J, Leyhausen G, Leibfritz D, Geurtsen W: Effect of TEGDMA on the intracellular glutathione concentration of human gingival fibroblasts. J Biomed Mater Res 2002, 63: 746-751.

17. Engelmann J, Janke V, Volk J, Leyhausen G, von Neuhoff N, Schlegelberger B, Geurtsen W: Effects of BisGMA on glutathione metabolism and apoptosis in human gingival fibroblasts in vitro. Biomaterials 2004, 25: 4573-4580.

18. Ferracane JL, Condon JR: Rate of elution of leachable components from composite. Dent Mater 1990, 6: 282-287.

19. Ferracane JL: Current trends in dental composites. Crit Rev Oral Biol Med 1995, 6: 302-319.

20. Finer Y, Santerre JP: Biodegradation of a dental composite by esterases: dependence on enzyme concentration and specificity. J Biomater Sci Polym Ed 2003, 14: 837-849.

21. Fotos PG, Diaz-Arnold AM, Williams VD: The effect of microbial contamination and pH changes in storage solutions during in vitro assays of bonding agents. Dent Mater 1990, 6: 154-157.

22. Freund M, Munksgaard EC: Enzymatic degradation of BISGMA/TEGDMA-polymers causing decreased microhardness and greater wear in vitro. Scand J Dent Res 1990, 98: 351-355.

23. Fujisawa S, Kadoma Y, Masuhara E: A calorimetric study of the interaction of synthetic phospholipid liposomes with vinyl monomers, acrylates and methacrylates.


J Biomed Mater Res 1984, 18: 1105-1114.

24. Fujisawa S, Kadoma Y, Komoda Y: 1H and '3C NMR studies of the interaction of eugenol, phenol, and triethyleneglycol dimethacrylate with phospholipid liposomes as


a model for odontoblast membranes. J Dent Res 1988, 67: 1438-1441.

25. Fujisawa S, Atsumi T, Kadoma Y: Cytotoxicity and phospholipid-liposome phase-transition properties of 2-hydroxyethyl methacrylate (HEMA). Artif Cells Blood Substit Immobil Biotechnol 2001, 29: 245–261.

26. Gerzina TM, Picker K, Hood A, Hume W: Toxicity and quantitative analysis of TEGDMA and composite resin eluates. J Dent Res 1991; 70 (suppl): 424.

27. Gerzina TM, Hume WR: Effect of dentine on release of TEGDMA from resin composite in vitro. J Oral Rehabil 1994, 21: 463–468.

28. Gerzina TM, Hume WR: Effect of hydrostatic pressure on the diffusion of monomers through dentin in vitro. J Dent Res 1995, vol. 74, 1: 369-373.

29. Geurtsen W, Spahl W, Leyhausen G: Residual monomer/additive release and variability in cytotoxicity of light-curing glass-ionomer cements and compomers. J Dent Res 1998a, 77: 2012-2019.

30. Geurtsen W, Lehmann F, Spahl W, Leyhausen G: Cytotoxicity of 35 composite monomers/additives in permanent 3T3- and three human oral primary fibroblast cultures. J Biomed Mater Res 1998b, 41: 474-480.

31. Geurtsen W, Leyhausen G: Chemical-biological interactions of the resin monomer triethyleneglycol-dimethacrylate (TEGDMA). J Dent Res 2001, 80: 2046-2050.

32. Gilchrist M, Thorsson V, Li B, Rust AG, Korb M, Kennedy K, Hai T, Bolouri H, Aderem A: Systems biology approaches identify ATF3 as a negative regulator of toll-like receptor 4. Nature 2006, 441: 173-178.

33. Gioka C, Bourauel C, Hiskia A, Kletsas D, Eliades T, Eliades G: Light-cured or chemically cured orthodontic adhesive resins? A selection based on the degree of cure, monomer leaching and cytotoxicity. Am J Orthod Dentofacial Orthop 2005, 127: 413-419.

34. Hanks CT, Strawn SE, Wataha JC, Craig RG: Cytotoxic effects of resin components on cultured mammalian fibroblasts. J Dent Res 1991, 70: 1450-1455.

35. Hansel C, Leyhausen G, Mai UE, Geurtsen W: Effects of various resin composite (co)monomers and extracts on two caries-associated micro-organisms in vitro. J Dent Res 1998, 77: 60–67.

36. Hardy K, Mansfield L, Mackay A, Benvenuti S, Ismail S, Arora P, O’Hare MJ, Jat PS: Transcriptional networks and cellular senescence in human mammary fibroblasts. Mol Biol Cell 2005, 16: 943-953.

37. He L, Simmen FA, Mehendale HM, Ronis MJ, Badger TM: Chronic ethanol intake impairs insulin signaling in rats by disrupting Akt association with the cell membrane. Role of TRB3 in inhibition of Akt/protein kinase B activation. J Biol Chem 2006, vol. 281, 16: 11126-11134.

38. Hegedus Z, Czibula A, Kiss-Toth E: Tribbles: novel regulators of cell function; evolutionary aspects. Cell Mol Life Sci 2006, 63: 1632-1641.

39. Hume WR, Gerzina TM: Bioavailability of components of resin-based materials which are applied to teeth. Crit Rev Oral Biol Med 1996, 7: 172-179.

40. Jackson PK: Linking tumor suppression, DNA damage and the anaphase promoting complex. Trends Cell Biol 2004, 14: 331-334.

41. Janke V, von Neuhoff N, Schlegelberger B, Leyhausen G, Geurtsen W: TEGDMA causes apoptosis in primary human gingival fibroblasts. J Dent Res 2003, 82: 814-818.

42. Kaina B: DNA damage-triggered apoptosis: critical role of DNA repair, double-strand breaks, cell proliferation and signaling. Biochem Pharmacol 2003, 66: 1547-1554.

43. Karin M, Ben-Neriah Y: Phosphorylation meets ubiquitination: the control of NF-κB activity. Annu Rev Immunol 2000, 18: 621- 663.

44. Kerley-Hamilton JS, Pike AM, Li N, DiRenzo J, Spinella MJ: A p53-dominant transcriptional response to cisplatin in testicular germ cell tumor-derived human embryonal carcinoma. Oncogene 2005, 24: 6090-6100.

45. Kleinsasser NH, Wallner BC, Harreus UA, Kleinjung T, Folwaczny M, Hickel R, Kehe K, Reichl FX: Genotoxicity and cytotoxicity of dental materials in human lymphocytes as assessed by the single cell microgel electrophoresis (comet) assay.


J Dent 2004, 32: 229-234.

46. Kleinsasser NH, Schmid K, Sassen AW, Harreus UA, Staudenmaier R, Folwaczny M, Glas J, Reichl FX: Cytotoxic and genotoxic effects of resin monomers in human salivary gland tissue and lymphocytes as assessed by the single cell microgel electrophoresis (comet) assay. Biomaterials 2006, 27: 1762-1770.

47. Larsen IB, Freund M, Munksgaard EC: Change in surface hardness of BisGMA/TEGDMA polymer due to enzymatic action. J Dent Res 1992, 71: 1851-1853.

48. Lefebvre CA, Schuster GS, Rueggeberg FA, Tamareselvy K, Knoernschild KL: Responses of oral epithelial cells to dental resin components. J Biomater Sci Polym Ed 1996, 7: 965-976.

49. Lefeuvre M, Bourd K, Loriot MA, Goldberg M, Beaune P, Perianin A, Stanislawski L: TEGDMA modulates glutathione transferase P1 activity in gingival fibroblasts.
J Dent Res 2004, 83: 914-919.

50. Lefeuvre M, Amjaad W, Goldberg M, Stanislawski L: TEGDMA induces mitochondrial damage and oxidative stress in human gingival fibroblasts. Biomaterials 2005, 26: 5130-5137.

51. Lin L, Qian Y, Shi X, Chen Y: Induction of a cell stress response gene RTP801 by DNA damaging agent methyl methanesulfonate through CCAAT/enhancer binding protein. Biochemistry 2005a, 44: 3909-3914.

52. Lin L, Stringfield TM, Shi X, Chen Y: Arsenite induces a cell stress response gene, RTP801, through reactive oxygen species and transcription factors Elk-1 and CCAAT/enhancer-binding protein. Biochem J 2005b, 392 (Pt 1): 93-102.

53. Machida YJ, Dutta A: The APC/C inhibitor, Emi1, is essential for prevention of rereplication. Genes Dev 2007, 21: 184-194.

54. Mackie EJ, Halfter W, Liverani D: Induction of tenascin in healing wounds. J Cell Biol 1988, 107: 2757-2767.

55. Mar L, Hoodless PA: Embryonic fibroblasts from mice lacking Tgif were defective in cell cycling. Mol Cell Biol 2006, 26: 4302-4310.

56. Mates JM, Sanchez-Jimenez FM: Role of reactive oxygen species in apoptosis: implications for cancer therapy. Int J Biochem Cell Biol 2000, 32: 157-170.

57. McCarthy TJ, Hayes EP, Schwartz CS, Witz G: The reactivity of selected acrylate esters toward glutathione and deoxyribonucleosides in vitro: structure-activity relationships. Fundam Appl Toxicol 1994, 22: 543-548.

58. Michelsen VB, Lygre H, Skalevik R, Tveit AB, Solheim E: Identification of organic eluates from four polymer-based dental filling materials. Eur J Oral Sci 2003, 111: 263-271.

59. Moszner N, Salz U: New developments of polymeric dental composites. Prog Polym Sci 2001, 26: 535-576.

60. Nishinaka Y, Masutani H, Oka S, Matsuo Y, Yamaguchi Y, Nishio K, Ishii Y, Yodoi J: Importin alpha1 (Rch1) mediates nuclear translocation of thioredoxin-binding protein-2/vitamin D(3)-up-regulated protein 1. J Biol Chem 2004, 279: 37559-37565.

61. Nishiyama A, Matsui M, Iwata S, Hirota K, Masutani H, Nakamura H, Takagi Y, Sono H, Gon Y, Yodoi J: Identification of thioredoxin-binding protein-2/vitamin D(3) upregulated protein 1 as a negative regulator of thioredoxin function and expression.
J Biol Chem 1999, 274: 21645-21650.

62. Nyberg KA, Michelson RJ, Putnam CW, Weinert TA: Toward maintaining the genome: DNA damage and replication checkpoints. Annu Rev Genet 2002, 36: 617-656.

63. Ortengren U: On composite resin materials-degradation, erosion and possible adverse effects in dentists. Swed Dent J 2000, 141 (suppl): 1-61.

64. Owens DM, Keyse SM: Differential regulation of MAP kinase signalling by dual-specificity protein phosphatases. Oncogene 2007, 26: 3203-3213.

65. Oyama F, Kotliarova S, Harada A, Ito M, Miyazaki H, Ueyama Y, Hirokawa N, Nukina N, Ihara Y: Gem GTPase and tau: morphological changes induced by gem GTPase in cho cells are antagonized by tau. J Biol Chem 2004, 279: 27272-27277.

66. Ozono R: New biotechnological methods to reduce oxidative stress in the cardiovascular system: focusing on the Bach1/heme oxygenase-1 pathway. Curr Pharm Biotechnol 2006, 7: 87-93.

67. Pande G: The role of membrane lipids in regulation of integrin functions. Curr Opin Cell Biol 2000, 12: 569-574.

68. Paranjpe A, Bordador LC, Wang MY, Hume WR, Jewett A: Resin monomer 2-hydroxyethyl methacrylate (HEMA) is a potent inducer of apoptotic cell death in human and mouse cells. J Dent Res 2005, 84: 172-177.

69. Patel SS, Walt DR: Acetyl coenzyme A synthetase catalyzed reactions of coenzyme A with alpha, beta-unsaturated carboxylic acids. Anal Biochem 1988, 170: 355-360.

70. Peutzfeldt A: Resin composites in dentistry: the monomer systems. Eur J Oral Sci 1997, 105: 97-116.

71. Piddini E, Schmid JA, de-Martin R, Dotti CG: The Ras-like GTPase Gem is involved in cell shape remodelling and interacts with the novel kinesinlike protein KIF9. EMBO J 2001, 20: 4076-4087.

72. Postek-Stefańska L: Wczesne obserwacje nad wpływem materiałów kompozytowych i ich systemów wiążących na miazgę zębową. Czas Stomatol 1996, XLIX, 8: 531-539.

73. Reichl FX, Durner J, Hickel R, Kunzelmann KH, Jewett A, Wang MY, Spahl W, Kreppel H, Moes GW, Kehe K, Walther U, Forth W, Hume WR: Distribution and excretion of TEGDMA in guinea pigs and mice. J Dent Res 2001, 80: 1412–1415.

74. Reichl FX, Durner J, Hickel R, Spahl W, Kehe K, Walther U, Gempel K, Liebl B, Kunzelmann KH, Hume WR: Uptake, clearance and metabolism of TEGDMA in guinea pigs. Dent Mater 2002, 18: 581–589.

75. Rowland BD, Bernards R, Peeper DS: The KLF4 tumour suppressor is
a transcriptional repressor of p53 that acts as a context-dependent oncogene. Nat Cell Biol 2005, 7: 1074-1082.

76. Rowland BD, Peeper DS: KLF4, p21 and context-dependent opposing forces in cancer. Nat Rev Cancer 2006, 6: 11-23.

77. Roy AA, Baragli A, Bernstein LS, Hepler JR, Hebert TE, Chidiac P: RGS2 interacts with Gs and adenylyl cyclase in living cells. Cell Signal 2006, 18: 336-348.

78. Rueggeberg FA, Margeson DH: The effect of oxygen inhibition on an unfilled/filled composite system. J Dent Res 1990, 69: 1652-1658.

79. Rueggeberg FA: From vulcanite to vinyl, a history of resins in restorative dentistry. J Prosthet Dent 2002, 87: 364-379.

80. Sancar A, Lindsey-Boltz LA, Unsal-Kacmaz K, Linn S: Molecular mechanisms of mammalian DNA repair and the DNA damage checkpoints. Annu Rev Biochem 2004, 73: 39-85.

81. Santerre JP, Shajii L, Leung BW: Relation of dental composite formulations to their degradation and the release of hydrolyzed polymeric-resin-derived products. Crit Rev Oral Biol Med 2001, 12: 136-151.

82. Schmalz G, Schweikl H, Hiller KA: Release of prostaglandin E2, IL-6 and IL-8 in human oral epithelial culture models after exposure to compounds of dental materials. Eur J Oral Sci 2000, 108: 442-448.

83. Schuster GS: Oral microbiology and infectious disease. 34th ed. B.C. Decker Inc.,Toronto, Kanada 1990: str. 472.

84. Schuster GS, Erbland JF, Lefebvre CA, Caughman GB, Knoemschild KL: Effects of an aminomethacrylate on the epithelial cell metabolism. J Biomater Sci Polym Ed 1997, 8: 363-375.

85. Schweikl H, Schmalz G, Rackebrandt K: The mutagenic activity of unpolymerized resin monomers in Salmonella typhimurium and V79 cells. Mutat Res 1998, 415: 119-130.

86. Schweikl H, Schmalz G: Triethylene glycol dimethacrylate induces large deletions in the hprt gene of V79 cells. Mutat Res 1999, 438: 71-78.

87. Schweikl H, Schmalz G, Spruss T: The induction of micronuclei in vitro by unpolymerized resin monomers. J Dent Res 2001, 80: 1615-1620.

88. Schweikl H, Altmannberger I, Hanser N, Hiller K-A, Bolay C, Brockhoff G, Spagnuolo G, Galler K, Schmalz G: The effect of triethylene glycol dimethacrylate on the cell cycle of mammalian cells. Biomaterials 2005, 26: 4111-4118.

89. Schweikl H, Spagnuolo G, Schmalz G: Genetic and cellular toxicology of dental resin monomers. J Dent Res 2006, 85: 870-877.

90. Schweikl H, Hartmann A, Hiller KA, Spagnuolo G, Bolay C, Brockhoff G, Schmaltz G: Inhibition of TEGDMA and HEMA-induced genotoxicity and cell cycle arrest by N-acetylcysteine. Dent Mater 2007, 23: 688-695.

91. Schweikl H, Hiller KA, Eckhardt A, Bolay C, Spagnuolo G, Stempfl T, Schmaltz G: Differential gene expression involved in oxidative stress response caused by triethylene glycol dimethacrylate. Biomaterials 2008, 29: 1377-1387.

92. Schwengberg S, Bohlen B, Kleinsasser N, Kehe K, Seiss M, Walther UI, Hickel R, Reichl FX: In vitro embryotoxicity assessment with dental restorative materials. J Dent 2005, 33: 49-55.

93. Seiss M, Nitz S, Kleinsasser N, Buters JT, Behrendt H, Hickel R, Reichl FX: Identification of 2,3-epoxymethacrylic acid as an intermediate in the metabolism of dental materials in human liver microsomes. Dent Mater 2007, vol. 23, 1: 9-16.

94. Seńczuk W: „Toksykologia współczesna”, Wydawnictwo Lekarskie PZWL, Warszawa 2005.

95. Shaulian E, Karin M: AP-1 as a regulator of cell life and death. Nat Cell Biol 2002, 4: E131-E136.

96. Simbulan-Rosenthal CM, Daher A, Trabosh V, Chen WC, Gerstel D, Soeda E, Rosenthal DS: Id3 induces a caspase-3- and -9-dependent apoptosis and mediates UVB sensitization of HPV16 E6/7 immortalized human keratinocytes. Oncogene 2006, 25: 3649-3660.

97. Song L, Jope RS: Cellular stress increases RGS2 mRNA and decreases RGS4 mRNA levels in SH-SY5Y cells. Neurosci Lett 2006, 402: 205-209.

98. Spagnuolo G, Galler K, Schmalz G, Cosentino C, Rengo S, Schweikl H: Inhibition of phosphatidylinositol 3-kinase amplifies TEGDMA-induced apoptosis in primary human pulp cells. J Dent Res 2004a, 83: 703-707.

99. Spagnuolo G, Mauro C, Leonardi A, Santillo M, Paternò R, Schweikl H, Avvedimento EV, Rengo S: NF-kappaB Protection against Apoptosis Induced by HEMA. J Dent Res 2004b, 83: 837-842.

100. Spagnuolo G, D’Antò V, Cosentino C, Schmalz G, Schweikl H, Rengo S: Effect of N-acetyl-L-cysteine on ROS production and cell death caused by hema in human primary gingival fibroblasts. Biomaterials 2006, 27: 1803-1809.

101. Spahl W, Budzikiewicz H: Qualitative analysis of dental resin composites by gas and liquid chromatography/mass spectrometry. Fresenius J Anal Chem 1994, 350: 684-691.

102. Stanislawski L, Lefeuvre M, Bourd K, Soheili-Majd E, Goldberg M, Perianin A: TEGDMA-induced toxicity in human fibroblasts is associated with early and drastic glutathione depletion with subsequent production of oxygen reactive species. J Biomed Mater Res 2003, 66: 476-482.

103. Tanaka J, Hashimoto T, Stansbury JW, Antonucci JM, Suzuki K: Polymer properties on resins composed of UDMA and methacrylates with the carboxyl group. Dent Mater J 2001, 20: 206–215.

104. Tang BL: Molecular genetic determinants of human brain size. Biochem Biophys Res Commun 2006, 345: 911-916.

105. Terakado M, Yamazaki M, Tsujimoto Y, Kawashima T, Nagashima K, Ogawa J, Fujita Y, Sugiya H, Sakai T, Furuyama S: Lipid peroxidation as a possible cause of benzoyl peroxide toxicity in rabbit dental pulp-a microsomal lipid peroxidation in vitro. J Dent Res 1984, 63: 901-905.

106. Theilig C, Tegtmeier Y, Leyhausen G, Geurtsen W: Effects of BisGMA and TEGDMA upon proliferation, migration, and tenascin expression of human fibroblasts and keratinocytes. J Biomed Mater Res 2000, 53: 632-639

107. Thomas EK, Nakamura M, Wienke D, Isacke CM, Pozzi A, Liang P: Endo180 binds to the C-terminal region of type I collagen. J Biol Chem 2005, 280: 22596-22605.

108. Thonemann B, Schmaltz G, Hiller KA, Schweikl H: Responses of L929 mouse fibroblasts, primary and immortalized dental papilla-derived cell lines to dental resin components. Dent Mater 2002, 18: 318-323.

109. Tsai MY, Wang S, Heidinger JM, Shumaker DK, Adam SA, Goldman RD, Zheng Y: A mitotic lamin B matrix induced by RanGTP required for spindle assembly. Science 2006, 311: 1887-1893.

110. van-de-Weerdt BC, Medema RH: Polo-like kinases: a team in control of the division. Cell Cycle 2006, 5: 853-864.

111. Varela-Rey M, Montiel-Duarte C, Oses-Prieto JA, Lopez-Zabalza MJ, Jaffrezou JP, Rojkind M, Iraburu MJ: p38 MAPK mediates the regulation of alpha1(I) procollagen mRNA levels by TNF-alpha and TGF-beta in a cell line of rat hepatic stellate cells. FEBS Lett 2002, 528: 133-138.

112. Walther UI, Siagian II, Walther SC, Reichl FX, Hickel R: Antioxidative vitamins decrease cytotoxicity of HEMA and TEGDMA in cultured cell lines. Arch Oral Biol 2004, 49: 125-131.

113. Wilder AD, Swift EJ, May KN, Thompson JY, McDougal RA: Effect of finishing technique on the microleakage and surface texture of resin-modified glass ionomer restorative materials. J Dent 2000, 28: 367-373.

114. Wu GS: The functional interactions between the p53 and MAPK signaling pathways. Cancer Biol Ther 2004, 3: 156-161.

115. Yoon HS, Chen X, Yang VW: Kruppel-like factor 4 mediates p53-dependent G1/S cell cycle arrest in response to DNA damage. J Biol Chem 2003, 278: 2101-2105.

116. Yoshida K: Identification and characterization of a novel kelch-like gene KLHL15 in silico. Oncol Rep 2005, 13: 1133-1137.

117. Yoshii E: Cytotoxic effects of acrylates and methacrylates: relationships of monomer structures and cytotoxicity. J Biomed Mater Res 1997, 37: 517-524.

118. Yourtee DM, Smith RE, Russo KA, Burmaster S, Cannon JM, Eick JD, Kostoryz EL: The stability of methacrylate biomaterials when enzyme challenged: kinetic and systematic evaluations. J Biomed Mater Res 2001, 57: 522–531.

119. Zhong X, Liu L, Zhao A, Pfeifer GP, Xu X: The abnormal spindle-like, microcephaly-associated (ASPM) gene encodes a centrosomal protein. Cell Cycle 2005, 4: 1227-1229.

120. Zimniak P, Nanduri B, Pikula S, Bandorowicz-Pikula J, Singhal SS, Srivastava SK, Awasthi S, Awasthi YC: Naturally occuring human glutathione-S-transferase GST P1-1 isoforms with isoleucine and valine in position 104 differ in enzymatic properties. Eur


J Biochem 1994, 204: 893-900.

RYCINY

1.

2.

Podpisy pod rycinami

Ryc. 1

Schemat cyto- i genotoksycznego działania TEGDMA na komórki ssaków.



Ryc. 2

Schemat cyto- i genotoksycznego działania HEMA na komórki ssaków








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