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  1. NTU Theses and Dissertations Repository
  2. 公共衛生學院
  3. 環境衛生研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42250
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dc.contributor.advisor林嘉明(Jia-Ming Lin)
dc.contributor.authorYi-Chen Chenen
dc.contributor.author陳儀貞zh_TW
dc.date.accessioned2021-06-15T00:55:26Z-
dc.date.available2013-09-11
dc.date.copyright2008-09-11
dc.date.issued2008
dc.date.submitted2008-08-04
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28. Mudzinski, S.P., Effects of benzo[a]pyrene on concanavalin a-stimulated human peripheral blood mononuclear cells in Vitro: inhibition of proliferation but no effect on parameters related to the G1 phase of the cell cycle. Toxicology and Applied Pharmacology. 1993. 119: 166-175.
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35. Yang, S.K., et al., Kinetic-analysis of metabolism of benzo[a]pyrene to phenols, dihydrodiols, and quinones by high-pressure chromatography compared to analysis by aryl-hydrocarbon hydroxylase assay, and effect of enzyme-induction. Cancer Research. 1975. 35(12): 3642-3650.
36. Reed, M.D., et al., Benzo[a]pyrene diones are produced by photochemical and enzymatic oxidation and induce concentration- dependent decreases in the proliferative state of human pulmonary epithelial cells. Journal of Toxicology and Environmental Health-Part A. 2003. 66(13): 1189-1205.
37. Landrum, P.F., et al., Bioaccumulation and critical body residue of PAHs in the amphipod, Diporeia spp.: Additional evidence to support toxicity additivity for PAH mixtures. Chemosphere. 2003. 51(6): 481-489.
38. Gon, Y., et al., Cooling and rewarming-induced IL-8 expression in human bronchial epithelial cells through p38 MAP kinase-dependent pathway. Biochemical and Biophysical Research Communications. 1998. 249(1): 156-160.
39. Moorthy, B., P. Sriram, and K. Randerath, Chemical structure-dependent and time-dependent effects of polycyclic aromatic hydrocarbon-type inducers on rat-liver cytochrome-P450, DNA-adducts, and I-compounds. Fundamental and Applied Toxicology. 1994. 22(4): 549-560.
40. Kim, S.Y., S.B. Hong, and J.H. Yang, Structure-dependent mechanism of action of poly aromatic hydrocarbons in cultured primary hepatocytes. Korean Society of Toxicology. 2006. 22(1): 23-30.
41. 李經民, et al., 南台灣K縣大氣中PAHs危害物質暴露之健康風險評估初探. 國立雲林科技大學環境與安全衛生工程系學刊. 2005. 6.
42. Woodruff, T.J., et al., Estimating cancer risk from outdoor concentrations of hazardous air pollutants in 1990. Environmental Research. 2000. 82(3): 194-206.
43. Komers, R., et al., Renal p38 MAP kinase activity in experimental diabetes. Laboratory Investigation. 2007. 87(6): 548-558.
44. Mrowietz U., et al., Anthralin (dithranol) in vitro inhibits human monocytes to secrete IL-6, IL-8 and TNF-α, but not IL-1. British Journal of Dermatology. 1997. 136: 542-547.
45. Carnaud C., et al., Cutting Edge: Cross-talk between cells of the innate immune system: NKT cells rapidly activate NK cells. The Journal of Immunology. 1999. 163: 4647-4650.
46. Meudec A., et al., Evidence for bioaccumulation of PAHs within internal shoot tissues by a halophytic plant artificially exposed to petroleum-polluted sediments. Chemosphere. 2006. 65(3): 474-481.
47. Shailaja M. S., et al., Formation of genotoxic nitro-PAH compounds in fish exposed to ambient nitrite and PAH. Toxicological Sciences. 2006. 91(2):440-447.
dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/42250-
dc.description.abstract本研究選擇具代表性的多環芳香烴化合物benzo[a]pyrene、phenanthrene、chrysene觀察人類支氣管上皮細胞(BEAS-2B cell),暴露該等多環芳香烴化合物後釋放激素interleukin-6(IL-6)及interleukin-8(IL-8)的效應。PAH暴露濃度設定為低(4.22~5.54 nM)、中(98.5~138.5 nM)、高(492.5~692.5 nM)三種範圍,暴露時間為8、12、16、24、48小時,IL-6及IL-8分析使用ELISA技術。結果發現,PAH的物種、濃度與暴露時間為影響細胞分泌IL-6與IL-8的重要變項。經暴露濃度歸一化調整後的IL-6、IL-8濃度,其單位時間的變化率隨PAH之物種而異,以benzo[a]pyrene較大。劑量-效應關係似乎呈現兩個階段,且因PAH物種而有差異:暴露benzo[a]pyrene,低劑量時IL-6、IL-8效應呈線性下降,相對較高劑量時反應隨劑量的平方而增加;而暴露phenanthrene或chrysene時,IL-6、IL-8的效應先呈線性的上升而後隨劑量的平方緩降。認為PAH造成細胞分泌細胞激素,產生發炎反應的影響可能存在,在濃度與暴露時間條件接近的情況下,不排除物種是關鍵因素。zh_TW
dc.description.abstractThis study aimed at evaluating the induction of interleukin-6(IL-6)and interleukin-8(IL-8)while the human bronchial epithelial cells, BEAS-2B cell, exposed to authentic benzo[a]pyrene, phenanthrene, and chrysene with concentration at low(4.22~5.54 nM), medium(98.5~138.5 nM), and high(492.5~692.5 nM)levels. The exposure lasted for 8, 12, 16, 24, and 48 hours, before the ELISA test were applied for detecting IL-6 and IL-8. The results demonstrated that the induction of IL-6 and IL-8 varied with species of PAH, concentration and exposure time. The change rate of cytokine level per hour exposure(pg/mL-nM/hr)varied with chemical species as the levels of IL-6 and IL-8 were normalized to exposure concentration. The change rate for benzo[a]pyrene was upmost. The does-effect relationship was interpreted by using linear-quadratic model assuming that the level of IL-6 or IL-8 is related to two phases of action. For benzo[a]pyrene, the level of IL-6 and IL-8 were negatively proportional to dose at the lower dose exposure and the level of IL-6 and IL-8 were positively proportional to the square of dose at the higher dose exposure. For exposure to phenanthrene or chrysene, the levels of IL-6 and IL-8 positively increase with the increment of dose at lower dose exposure and then slightly decrease with the square of dose at higher dose exposure. The induction of proinflammatory cytokines in epithelial cell likely occurs due to exposure to polynuclear aromatic hydrocarbons, and the effects mainly depend on chemical species as the other exposure modifiers such as exposure concentration and exposure time are identical.en
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Previous issue date: 2008
en
dc.description.tableofcontents致謝I
摘要II
AbstractIII
目錄IV
表列VI
圖列VII
第一章 緒論1
一. 前言1
二. 研究目的2
三. 研究架構3
第二章 文獻回顧4
一. 環境中的多環芳香烴化合物4
二. 空氣污染對氣喘發生之影響4
三. 呼吸系統的發炎反應5
四. 多環芳香烴化合物對健康之影響6
五. 人類呼吸系統免疫機制8
第三章 材料與方法10
一. 材料10
二. 方法12
化學物質多環芳香烴的濃度配製12
細胞暴露實驗12
細胞繼代培養12
細胞密度計數15
接種(Seeding)16
細胞暴露17
ELISA分析17
三. 資料處理19
第四章 結果與討論20
一. 暴露時間、暴露濃度對BEAS-2B cell分泌IL-6與IL-8的影響20
二. 細胞分泌IL-6、IL-8對於暴露PAH單位濃度、暴露時間與PAH物種的反應21
三. IL-6、IL-8與PAHs暴露劑量(時間×濃度)的關係24
四. PAH大氣樣品對細胞分泌IL-6、IL-8濃度影響25
五. 研究的限制與建議26
參考文獻28
附錄
表列
表一.多環芳香烴的濃度配製34
表二.BEAS-2B細胞株詳細資料34
表三.BEAS-2B cell暴露benzo[a]pyrene分泌IL-6、IL-8之結果35
表四.BEAS-2B cell暴露Phenanthrene分泌IL-6、IL-8之結果37
表五.BEAS-2B cell暴露Chrysene分泌IL-6、IL-8之結果39
表六.BEAS-2B cell分泌IL-6與PAH物種、濃度分組及暴露時間的關係41
表七.BEAS-2B cell分泌IL-8與PAH物種、濃度分組及暴露時間的關係42
表八.IL-6濃度與暴露時間的指數關係43
表九.IL-8濃度與暴露時間的指數關係44
圖列
圖一.BEAS-2B cell 分泌IL-6與PAH物種、濃度分組及暴露時間的關係45
圖二.BEAS-2B cell 分泌IL-8與PAH物種、濃度分組及暴露時間的關係46
圖三.高濃度PAH暴露下IL-6反應與暴露時間的關係47
圖四.中濃度PAH暴露下IL-6反應與暴露時間的關係48
圖五.低濃度PAH暴露下IL-6反應與暴露時間的關係49
圖六.高濃度PAH暴露下IL-8變化與暴露時間的關係50
圖七.中濃度PAH暴露下IL-8濃度變化與暴露時間的關係51
圖八.低濃度PAH暴露下IL-8濃度變化與暴露時間的關係52
圖九.IL-6效應與PAH暴露劑量(濃度×時間)的關係53
圖十.IL-8效應與PAH暴露劑量(濃度×時間)的關係54
dc.language.isozh-TW
dc.subject第八介白素zh_TW
dc.subject多環芳香烴化合物zh_TW
dc.subjectbnzo(a)pyrenezh_TW
dc.subjectphenanthrenezh_TW
dc.subjectchrysenezh_TW
dc.subject第六介白素zh_TW
dc.subjectinterleukin-6en
dc.subjectinterleukin-8en
dc.subjectpolynuclear aromatic hydrocarbons(PAHs)en
dc.subjectbnzo(a)pyreneen
dc.subjectphenanthreneen
dc.subjectchryseneen
dc.titleBenzo[a]pyrene、Phenanthrene、Chrysene誘導人類支氣管上皮細胞BEAS-2B Cell表現interleukin-6與 interleukin-8zh_TW
dc.titleInterleukin-6 and Interleukin-8 Induced by Benzo[a]pyrene、Phenanthrene、Chrysene in Human Bronchial Epithelial BEAS-2B Cellen
dc.typeThesis
dc.date.schoolyear96-2
dc.description.degree碩士
dc.contributor.oralexamcommittee蔡詩偉(Shih-Wei Tsai),謝玲玲(Ling-Ling Hiseh)
dc.subject.keyword多環芳香烴化合物,bnzo(a)pyrene,phenanthrene,chrysene,第六介白素,第八介白素,zh_TW
dc.subject.keywordpolynuclear aromatic hydrocarbons(PAHs),bnzo(a)pyrene,phenanthrene,chrysene,interleukin-6,interleukin-8,en
dc.relation.page76
dc.rights.note有償授權
dc.date.accepted2008-08-05
dc.contributor.author-college公共衛生學院zh_TW
dc.contributor.author-dept環境衛生研究所zh_TW
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