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研究生：	王伯智 Wang, Bour-Jr
論文名稱：	金屬鉻皮膚過敏性接觸性皮膚炎致病機轉之研究 Mechanisms of Chromium Hypersensitivity
指導教授：	王應然 Wang, Ying-Jan
學位類別：	博士 Doctor
系所名稱：	醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health
論文出版年：	2010
畢業學年度：	98
語文別：	中文
論文頁數：	95
中文關鍵詞：	六價鉻、鉻過敏性接觸性皮膚炎、腫瘤壞死因子-α 、N-乙醯基半胱胺酸、自由基
外文關鍵詞：	Hexavalent chromium, chromium hypersensitivity, tumor necrosis factor, N-acetylcysteine, reactive oxygen species
相關次數：	點閱：129 下載：2
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國內建築業勞工約80萬人佔全部勞動人口的12%，其重大職業災害發生率佔全產業全部重大職業災害發生率60%以上，而其中職業性皮膚病盛行率為21%居所有職業病之冠。水泥工工人的職業性皮膚炎主要可以分為二種，一是刺激性接觸性皮膚炎，另一種是過敏性接觸性皮膚炎。而過敏性接觸性皮膚炎最常見的過敏原是六價鉻。根據郭育良教授的研究，台南縣市的水泥工中男性有16.5%對鉻過敏而女性為7.2%皆高出一般人許多倍。水泥工一旦對鉻產生過敏性接觸性皮膚炎後其皮膚症狀通常會較單純的刺激性接觸性皮膚炎的水泥工為嚴重，預後也不好，且手部皮膚病變很容易復發。因此了解水泥工對鉻產生過敏性接觸性皮膚炎的致病機轉及如何保護水泥工手部免於對鉻產生過敏性接觸性皮膚炎是一個很重要的課題。然而我們對鉻產生過敏性接觸性皮膚炎的致病機轉，至今尚未清楚的了解。本研究的目的在了解六價鉻導致皮膚過敏致病的分子機轉並嘗試找出有潛力的藥物可用來預防水泥工對鉻發生鉻過敏性接觸性皮膚炎；同時也由基因的角度來看那些水泥工比較會對鉻產生過敏性接觸性皮膚炎。
經研究我們發現六價鉻在人類的表皮細胞及天竺鼠的皮膚可以導致自由基的生成及增加，繼而導致Akt、NF-kB及MAPK細胞傳遞訊息的活化及腫瘤壞死因子-α及介白素1-α生成的增加；而已知腫瘤壞死因子-α及介白素1會影響蘭格罕氏細胞的成熟及由表皮遷移至體內淋巴結，且是皮膚接觸性皮膚炎產生的關鍵。
我們也發現在鉻致敏的動物模式中，餵以N-乙醯基半胱胺酸，分析其皮膚及血漿中的自由基，發現N-乙醯基半胱胺酸可以降低過氧化氫及丙二醛的形成及提高天竺鼠血漿中的總抗氧化能力。另外餵以N-乙醯基半胱胺酸也可抑制其皮膚鉻過敏發炎的嚴重程度，且可有效的抑制天竺鼠對鉻皮膚過敏的產生。因此我們認為N-乙醯基半胱胺酸是一種有潛力可用來預防鉻皮膚過敏產生的藥物。
至於有關水泥工中患有鉻過敏性接觸性皮膚炎及沒有鉻過敏性接觸性皮膚炎的基因是否有所不同是我們有興趣的另一重點。我們發現水泥工如果是有腫瘤壞死因子-α G/A 308基因型和不具麩胺基硫-S-轉移酶-T基因型時較易產生鉻過敏性接觸性皮膚炎。
由以上的發現，我們將進一步探討六價鉻在過敏性接觸性皮膚炎致病機轉中所扮演的角色，包括使用不同的抗氧化劑及各種不同的細胞傳遞訊息的抑制劑及不同的抗細胞激素物質來了解其確實的詳細機轉及尋求更有效的預防鉻過敏性接觸性皮膚炎的藥物。我們也將利用這些已建立的動物模式、實驗方法及技術，進一步了解其他常見的環境及職業相關過敏原如金屬鎳、鈷、香料等的皮膚過敏機轉及尋求更好的治療及預防的方法，以幫助為數眾多的此類病患並保障及促進他們的皮膚健康。

In Taiwan, the number of construction workers is about 8 hundred thousand, which represents 12% of the total working population. In previous studies, the prevalence of occupational skin diseases among construction workers was as high as 21%. It was the leading cause of occupational diseases in Taiwan. The majority of construction workers are cement workers and irritant cement contact dermatitis and allergic cement contact dermatitis rate as two of the most prevalent occupational dermatoses. The major cause of allergic cement contact dermatitis is hexavalent chromium. The prevalence of chromium hypersensitivity in Taiwanese cement workers was shown to be around 13%, which is more than twenty- fold when compared to the general population. The prognosis of chromium hypersensitivity is poor and workers who are continually exposed to cement are susceptible to its repeated recurrence. The detailed pathogenesis of chromium hypersensitivity remains unknown. The aims of our study are to investigate the pathogenic molecular mechanisms of chromium hypersensitivity, attempt to find potential chemopreventative agents to prevent the development of chromium hypersensitivity, as well as to discover the genetic background for cement workers with a chromium hypersensitivity disposition.
We found that hexavalent chromium could increase ROS formation, activate the Akt, NF-kB, and MAPK pathways, as well as increase the production of cytokines, including TNF-α and IL-1α in keratinocytes. The release of these cytokines from keratinocytes is considered to be a key participant in the pathogenesis of contact hypersensitivity.
In addition, we clearly demonstrated, in a coadjuvant chromium-sensitized albino guinea pig model, that the use of NAC could effectively reduce H2O2 and MDA levels in skin, increase the ORAC in plasma, and significantly decrease the sensitization rate of chromium hypersensitivity, Therefore, NAC could be a potential agent to prevent the development of chromium hypersensitivity in those workers who are unavoidably exposed to work-related chromium.
With regards to the genetic background of cement workers prone to chromium hypersensitivity, we found a genetic predisposition of TNF-α-308 GA genotype and GST-T1 null genotype to chromium sensitization.
Future studies will focus on the detailed molecular mechanisms of hexavalent chromium on keratinocytes by utilizing different types of antioxidants and specific Akt, NF-kB, MAPK inhibitors and anti-cytokines, to elucidate the relationships between ROS, cell signaling pathways and cytokine production in keratinocytes after exposure to hexavalent chromium. We would also like to utilize these new findings, plus well-established animal models and laboratory techniques to find out the detailed mechanisms of contact hypersensitivity with regards other common environmental or occupational related allergens, such as nickel, cobalt and fragrances, as well as probe new possible therapeutic and chemopreventative agents to help those who are subjected to regular contact with these allergens.

誌謝...............................................................................................................................I
中文摘要.......................................................................................................................II
Abstract.................................................................................................................III-IV
Abbreviations. ....................................................................................................X-XI
Publication list ........................................................................................................XII
Introduction..................................................................................................................1
Occupational skin diseases in cement workers and chromium hypersensitivity..1
Mechanism of contact hypersensitivity…………………………………...……… 2
Chromium toxicity......................................................................................................3
Hexavalent chromium, ROS, cell signaling and cytokines.....................................4
Antioxidants and N-acetylcysteine............................................................................5
Animal model and HaCaT cells................................................................................6
Genetic polymorphism study.....................................................................................7
Objectives.....................................................................................................................9
Materials and Methods..............................................................................................10
Subjects....................................................................................................................10
Animals.....................................................................................................................10
Materials..................................................................................................................11
HaCaT cells culture.................................................................................................12
MTT cell viability assay..........................................................................................12
Measurement of intracellular hydrogen peroxide/ROS formation in HaCaT
cells...........................................................................................................................13
Western blot analysis..............................................................................................13
Measurement of TNF-α mRNA and IL-1α mRNA by reverse
transcription–polymerase chain reaction in HaCaT cells...................................14
VI
Detection of IL-1α by ELISA in HaCaT cells.......................................................15
Analysis of H2O2 levels in the skin of albino GP...................................................16
Detection of the epidermal protein expression of the Akt, NF-κB and MAPK
pathways in the epidermis of albino GP................................................................16
Detection of the expression of TNF-α and IL-1α in the epidermis of albino
GP.............................................................................................................................17
Administration of NAC and the coadjuvant chromium sensitization method..18
Intradermal and Epicutaneous Elicitation test....................................................19
Skin specimens and plasma for the determination of H2O2, MDA and
ORAC.......................................................................................................................20
Determination of H2O2 levels in skin of GP from Groups D-J..........................21
Determination of MDA levels in skin of GP from Groups D-J...........................21
Determination of ORAC in the plasma of GP from Groups D-J........................22
Histological examinations of the GP skin..............................................................23
Genetic polymorphisms study................................................................................23
Statistical analysis...................................................................................................23
Results........................................................................................................................25
MTT cell viability assay in HaCaT cells.............................................................25
Cr(VI) induced hydrogen peroxide/ROS generation in HaCaT cells..............25
Cr(VI) activated the Akt, NF-κB and MAPK pathways in HaCaT cells........26
Cr(VI) increased the expression of TNF-α mRNA in HaCaT cells..................27
Cr(VI) increased the release of IL-1α and the expression of IL-1α mRNA in
HaCaT cells...........................................................................................................27
Cr(VI) dermal injection increased H2O2 formation, activated the Akt, NF-κB,
MAPK pathways, and induced the expression of TNF-α and IL-1α in the skin
VII
of albino GP..........................................................................................................28
NAC administration diminished the severity of skin reaction in the
intradermal elicitation test..................................................................................29
NAC administration diminished the severity of skin reaction in the
epicutaneous elicitation test and reduced the sensitization rate of chromium
hypersensitivity.....................................................................................................29
NAC decreased H2O2 levels in the skin of chromium and/or FCA
injected GP............................................................................................................30
NAC decreased MDA levels in the skin of chromium- and/or FCA-injected
GP...........................................................................................................................31
NAC increased ORAC levels in the plasma of chromium and/or FCA injected
GP...........................................................................................................................32
Histological examination showed that NAC could inhibit the eczematous
reaction in coadjuvant chromium-sensitized GP...............................................32
Demographic data, the location, and prevalence of dermatitis in cement
workers…………………………………………………………………….…….33
Prevalence and involved sites of reported skin diseases in cement workers.. 33
Genotype frequencies at the TNF-a-308, IL-4-590, GST-T1, and GST-M1 in
cement workers………………………………………………………………..34
The risk genotype for skin sensitization to hexavalent chromium in cement
workers…………………………………………………………………………34
Discussion...................................................................................................................35
References...................................................................................................................48
Tables..........................................................................................................................62
Figures........................................................................................................................68
VIII
Appendix 1................................................................................................................88
Appendix 2................................................................................................................89
Appendix 3................................................................................................................90
Appendix 4................................................................................................................91
Appendix 5................................................................................................................92
Appendix 6................................................................................................................93
Appendix 7................................................................................................................94
Appendix 8................................................................................................................95
IX
Table and Figure List
Table 1........................................................................................................................62
Table 2........................................................................................................................63
Table 3........................................................................................................................64
Table 4........................................................................................................................65
Table 5........................................................................................................................66
Table 6........................................................................................................................67
Figure 1.......................................................................................................................68
Figure 2...................................................................................................................69,70
Figure 3a.....................................................................................................................71
Figure 3b.....................................................................................................................72
Figure 4.......................................................................................................................73
Figure 5a.....................................................................................................................74
Figure 5b,c..................................................................................................................75
Figure 6a......................................................................................................................76
Figure 6b.....................................................................................................................77
Figure 6c,d...................................................................................................................78
Figure 7...................................................................................................................79,80
Figure 8...................................................................................................................81,82
Figure 9a..................................................................................................................... 83
Figure 9b.....................................................................................................................84
Figure 9c......................................................................................................................85
Figure 10.................................................................................................................86,87
                                    

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