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研究生:張寧家
研究生(外文):Ning-Chia Chang
論文名稱:影響台灣勞工噪音性聽力障礙易感性相關因子之研究
論文名稱(外文):Factors Associated with the Susceptibility to Noise-Induced Hearing Loss in Taiwan
指導教授:何坤瑤何坤瑤引用關係
指導教授(外文):Kuen-Yao Ho
學位類別:博士
校院名稱:高雄醫學大學
系所名稱:醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2011
畢業學年度:99
語文別:中文
論文頁數:102
中文關鍵詞:噪音性聽損高血脂症活性氧族超氧化物岐化脢熱休克蛋白基因多型性
外文關鍵詞:Noise-induced hearing losshyperlipidemiareactive oxygen speciessuperoxide dismutaseheat shock proteingenetic polymorphism
相關次數:
  • 被引用被引用:1
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噪音性聽障為常見之聽力損傷,而不同個體有不同的噪音性聽損易感性;本報告的研究方向在於尋找可能造成個體間噪音性聽損易感性差異的因子。研究分析噪音暴露之下的工廠勞工之生化數值與聽力損傷的關係,發現血中空腹三酸甘油酯數值≥150 mg/dL者,有較高的機會罹患聽力損傷(aOR=1.281,95% CI=1.088-1.507);由此推測血脂代謝過程所產生的自由基及活性氧族(ROS)與噪音易感性有關,進而研究超氧化物岐化脢族群中的manganese SOD (SOD2)與噪音性聽障易感性的相關性,發現SOD2多型性基因rs2758332中基因型為G/T者,比帶有同質對偶基因型者對噪音更具易感性(aOR=5.367,95% CI=1.359-21.205)。被ROS破壞的細胞之DNA與蛋白質,需要如熱休克蛋白(HSP)等酵素來修復,於是研究HSP70基因家族中的多型性基因(rs2075800, rs1043618, rs2763979),發現其中rs1043618基因為G/C的受檢者對噪音有比較高的易感性(aOR=2.634; 95% CI=1.096 – 6.328),同時發現帶有CCC組合的單倍型(haplotype)之受檢者對噪音亦有比較高的敏感性(OR=2.197; 95% CI=1.110 – 4.370),推測熱休克蛋白70的多型性基因與噪音性聽障的易感性有關。利用本系列研究的結果及模式,可篩檢出對噪音性聽損較具易感性的人員,作為噪音性聽障預防之參考,以降低噪音性聽障之盛行率。

Noise-induced hearing loss (NIHL) is a common acquired hearing loss in adults. Previous studies found that individuals exhibit different susceptibility to NIHL. The objectives of this series of studies were to investigate the factors associated with the susceptibility to NIHL in the Taiwanese population.
The subjects of this series of studies were from the factories by which the Department of Preventive Medicine, Kaohsiung Medical University Hospital was committed to perform annual health examinations. All the participants were exposed to occupational noise exceeding 85 dBA. In the initial study, we found that individuals with serum triglyceride level ≥150 mg/dL were prone to a 28% increased risk to have NIHL in comparison with those whose serum triglyceride level <150 mg/dL. It was speculated that the metabolism of excessive triglyceride would produce a large amount of free radicals and reactive oxygen species (ROS). Based on the pathogenesis of NIHL, ROS were the major substances responsible for DNA and protein damage leading to apoptosis, whereas superoxide dismutases (SODs) and heat shock proteins (HSPs) played protective roles to prevent cell death. The association of SOD2 single nucleotide polymorphism (SNP) IVS3-23T/G (SNP No.: rs2758332) with NIHL susceptibility was investigated. It was found that individuals with T/G genotype of SNP IVS3-23T/G were significantly more vulnerable to noise (aOR=6.222; 95%CI=1.498 – 25.855) than the wild type (i.e. T/T). The relationships between three SNPs of the hsp70 family (rs2075800; rs1043618, rs2763979) and NIHL were also analyzed. The G/C genotype of SNP rs1043618 was found to be associated with NIHL susceptibility (aOR=2.634; 95% CI=1.096 – 6.328). Analysis of haplotypes composed of these three SNPs revealed a significant association between NIHL susceptibility and haplotype CCC (OR=2.197; 95% CI=1.110 – 4.370). Thus the genetic polymorphisms in the SOD2 and HSP70 genes were thought to be associated with the individual’s susceptibility to NIHL in the Taiwanese population.
This serial of studies established the data of the relationships between some genetic polymorphisms and NIHL susceptibility in the Taiwanese population. The reults in these studies supported the hypothesis that ROS plays a crucial destructive role, whereas SOD2 and HSPs play the protective roles in the pathogenesis of NIHL. These findings could be used as a reference in the understanding and the prevention of NIHL.


誌謝 i
中文摘要 ii
Abstract iii
前言 1
研究背景、目的及重要性 4
研究對象及方法 7
研究內容 9
研究子題一:高血脂症與噪音暴露對聽力影響的相關性 9
材料與方法 9
結果 10
討論 12
附表 16
Table 1 16
Table 2 17
研究子題二:錳-超氧化物岐化脢(SOD2)基因多型性與噪音易感性之關係 18
材料與方法 19
結果 22
討論 23
附表 28
Table 3 28
Table 4 29
研究子題三:熱休克蛋白多型性基因與噪音性聽損易感性之關係 30
材料與方法 33
結果 38
討論 39
附表 45
Table 5 45
Table 6 46
Table 7 47
Table 8 49
?鬖X討論 50
受檢者募集與噪音暴露劑量資料 51
定義噪音性聽損易感性表現型 52
抗氧化酵素及其基因多型性與噪音性聽損之關係 58
Superoxide Dismutase 60
Glutathione及其代謝相關酵素 65
Catalase 67
熱休克蛋白及其基因多型性與噪音性聽損之關係 70
研究成果、臨床應用及未來發展 76
參考文獻 80
附註 95


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