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研究生:郭志宏
研究生(外文):Chih-Hung Guo
論文名稱:鋁誘發雄性生殖系統毒性之機制
論文名稱(外文):The Mechanism of Aluminum-Induced Male Reproductive Toxicity
指導教授:王果行王果行引用關係
指導教授(外文):Guoo-Shyng Wang Hsu
學位類別:博士
校院名稱:輔仁大學
系所名稱:食品營養學系
學門:醫藥衛生學門
學類:營養學類
論文種類:學術論文
論文出版年:2001
畢業學年度:89
語文別:英文
論文頁數:206
中文關鍵詞:一氧化氮合成酶生精作用睪固酮炎症反應氧化壓力
外文關鍵詞:AluminumNitric oxide synthaseSpermatogenesisTestosteroneInflammatory reactionOxidative stress
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因高鋁誘發雄性生殖系統毒性之機制仍不清楚。本論文就氯化鋁對
雄性生殖毒性作深入探討。以腹腔注射給予 CD-1 雄性小白鼠不同劑量之氯化鋁 (2 週),分成對照組 (0 mg Al/kg/day)、低鋁 (7 mg Al/kg/day)、中鋁 (13 mg Al/kg/day)、及高鋁 (35 mg Al/kg/ day) 四組。結果發現鋁毒性可能直接作用在睪丸組織。在低鋁組並未發現毒性作用,但中鋁及高鋁組之生精 (spermatogenesis)、固醇生成作用 (steroidogenesis)、與生殖表現則明顯較對照組差。鋁聚積在睪丸組織明顯誘發相對組織位置的誘發型一氧化氮合成酶 (inducible nitric oxide synthase, iNOS) 之蛋白及 mRNA 表現,過量的一氧化氮產物 (NO) 與睪固酮 (testosterone) 濃度呈明顯之負相關性。混合投予高鋁與 iNOS 抑制劑 (L-NIL, 20 mg/kg/day, 12 days) 組其睪丸組織的 NO 產物較單獨投予高鋁組為低,然而睪固酮濃度明顯較高。顯示鋁誘發 iNOS 產生過量之 NO,造成睪固酮的合成分泌明顯被抑制。然而,鋁誘發 NO 形成亦與炎症反應 (inflammatory reaction) 有關。高鋁組睪丸組織有較低的 cyclic AMP、及膽固醇支鏈裂解酶(cholesterol side-chain cleavage enzyme, p-450scc)、與較高的膽固醇含量,推測因鋁誘發 NO 產物抑制 cyclic AMP,使得較少的膽固醇進入粒腺體,並抑制 p-450scc 使得膽固醇無法進一步裂解。此外,過高的 NO 可以增加鋁對於膜的通透性,造成組織內聚積較高的鋁濃度。本論文亦發現,睪丸組織有較低的鋅、與較高的鐵及銅離子,組織的脂質過氧化指標 (thiobarbituric acid-reactive substances, TBARS) 顯著較高。建議高鋁環境改變睪丸組織的離子代謝並增加氧化壓力。
The precise mechanisms of aluminum (Al)-induced male reproductive toxicity remain to be elucidated. The present investigations have been conducted on the reproductive toxicity in adult males exposed to Al. Al chloride was intraperitoneal administered to male mouse at doses of 0, 7, 13, and 35 mg Al/kg/day for 2 weeks (designated as C, LAL, MAL and HAL) respectively. The results suggested that Al exerted its toxic effect directly at the testis rather than hypothalamus-pituitary. Significantly detrimental effects on spermato- genesis, steroidogenesis and reproductive performance were found at LAL and HAL groups. The induction of inducible nitric oxide synthase (iNOS) protein over-expression and -transcription in testis was corresponded to Al accumulation. Increasing production of NO, induced by accumulated Al, was negative correlated to testosterone levels. Administrating Al with iNOS inhibitor (L-NIL, 20 mg/kg/day) for a period of 12 days, decreased the NO products and elevated testosterone levels. This result confirmed that Al depressed testosterone through inducing NO production. However, an inflammatory reaction might be involved in Al-induced excessive NO products. The results of decreased cyclic AMP and interfered the activation of cholesterol side-chain cleavage enzyme (p-450scc) implicated that Al might decrease the across of cholesterol through mitochondrial membrane by Al accumulation in testis. In addition, excessive NO increased the permeability of organism membrane for Al, possibly involved in more Al accumulation. The present study also showed that high level of Al resulted in lower zinc and higher iron, copper and TBARS (thiobarbituric acid-reactive substances) levels in the testis of mice. It was suggested that the Al intoxication associated with the occurrence of abnormal mineral metabolism and increasing oxidative stress in the testes of mice.
中文摘要Ⅰ
英文摘要Ⅱ
第一章 緒論 1
第二章 文獻回顧 2
壹、鋁
1.1. 鋁之特性 3
1.2. 鋁毒性之臨床特徵 4
1.3. 影響鋁吸收之因素 6
1.4. 鋁毒性與貧血 7
1.5. 鋁毒性對神經細胞或神經發育的影響 9
1.6. 鋁對動物母體及其子代發育之毒性 11
1.7. 鋁對於雄性生殖系統之毒性 14
1.8. 鋁毒性之可能機制 15
貳、一氧化氮
2.1. 一氧化氮合成酶之特性 19
2.2. 一氧化氮與脂質過氧化之發生 22
2.3. 一氧化氮對母體及子代之毒性作用 24
2.4. 一氧化氮對雄性生殖系統之毒性作用 25
一氧化氮引起精細胞死亡 25
一氧化氮抑制雄性激素的合成與分泌 26
一氧化氮抑制類脂醇生合成酵素之表現 27
一氧化氮抑制腦下腺的激素分泌 28
2.5. 一氧化氮與貧血 29
一氧化氮誘發血基質的瓦解 30
一氧化氮降低鐵蛋白的鍵結能力 30
一氧化氮改變參與血紅素生成酵素之活性 32
第三章 探討之問題與進行之方向 34
第四章 鋁誘發雄性小白鼠生殖系統之毒性
中文摘要36
英文摘要37
前言38
材料與方法38
結果41
討論42
圖表44
第五章 鋁誘發睪丸組織的一氧化氮產物及降低睪固酮濃度
中文摘要49
英文摘要50
前言51
材料與方法51
結果52
討論53
圖表57
第六章 鋁聚積在睪丸組織與誘發一氧化氮合成酶表現
中文摘要61
英文摘要62
前言63
材料與方法63
結果72
討論74
圖表76
第七章 鋁誘發一氧化氮產物抑制睪丸組織的固醇生成作用
中文摘要81
英文摘要82
前言83
材料與方法83
結果85
討論86
圖表89
第八章 鋁毒性致睪丸組織產生發炎反應及抑制睪固酮濃度
中文摘要93
英文摘要94
前言95
材料與方法95
結果97
討論97
圖表99
第九章 鋁毒性改變睪丸組織的離子分佈與誘發氧化壓力
中文摘要103
英文摘要104
前言105
材料與方法105
結果106
討論107
圖表110
第十章 參考文獻114
第十一章 著作發表156
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