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研究生:李怡芬
研究生(外文):Yi-Fen Lee
論文名稱:三氧化二砷對MPTP所引發之神經毒性效應
論文名稱(外文):Effects of Arsenite on MPTP-induced neurotoxicity in CNS
指導教授:林滿玉
指導教授(外文):Anya Maan-Yuh Lin
學位類別:碩士
校院名稱:國立陽明大學
系所名稱:生理學研究所
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:2004
畢業學年度:92
語文別:中文
論文頁數:67
中文關鍵詞:三氧化二砷細胞凋亡烏腳病過氧化氫催化酵素大腦皮質中樞神經系統
外文關鍵詞:As2O3AsApoptosisBlackfoot diseasecatalaseCerebral cortexcentral nervous system
相關次數:
  • 被引用被引用:1
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三氧化二砷 (As2O3, As) 在環境中被視為一種有毒物質,長期飲用含砷飲水會導致慢性砷中毒,造成心血管疾病、癌症及神經系統異常。三氧化二砷所引發的毒性為氧化壓力的產生,包括反應性氧族的形成、脂質過氧化的增加,進一步導致細胞死亡。在中樞神經系統,當人類暴露於急性砷的環境下,會引發腦病變;暴露於慢性砷的環境下,會導致認知缺陷、末梢神經退化、髓鞘脫失。利用神經退化性疾病之一的巴金森氏症的動物模式,來探討三氧化二砷是否影響1-methyl-4-phenyl-1,2,3,6-tetrapyridine(MPTP)一種具有選擇性的多巴胺神經毒素之神經毒性。雄性且成年的BALB/c 小鼠,分為solvent+saline(控制組)、solvent+MPTP(MPTP處理組)、As+saline(As處理組)及As+MPTP(As+MPTP處理組)四個組別。其中每天管餵三氧化二砷(6 mg/kg/day)或solvent連續21天,最後的7天以腹腔注射的方式給予MPTP(20 mg/kg)或是生理食鹽水(0.2ml)。實驗結果顯示: MPTP、As和As+MPTP皆不會影響小鼠體重。離體實驗(in vitro)發現, 慢性MPTP 和As並沒有影響大腦皮質均質液之auto-oxidation和 iron-induced脂質過氧化程度,As+MPTP組其auto-oxidation 和iron-induced 脂質過氧化程度明顯低於control 組。體內實驗(in vivo)發現:單獨As不會影響紋狀體的多巴胺含量,單獨給予MPTP明顯降低紋狀體的多巴胺含量,然而As會加強MPTP紋狀體多巴胺含量的減少。同時,免疫組織化學染色法的結果顯示,As會加強MPTP降低黑質核的酪胺酸氫氧化酵素(tyrosine hydroxylase)之免疫染色。此外,單獨MPTP 、As或As+MPTP不會改變紋狀體的GSH含量和GPx活性。但單獨MPTP或As則降低紋狀體Catalase活性。在分子學層面上,單獨As不會影響Bcl-2表現,但會增加黑質核內Bax表現,且降低Bcl-2/Bax之ratio。但As對MPTP降低Bcl-2/Bax ratio並無影響。根據實驗結果,As可能會加強MPTP在黑質核紋狀體多巴胺神經系統所引發的神經毒性,此作用並不經過GSH, GPx and Bcl-2途徑。
Arsenic trioxide (As2O3, As) is one of the global environmental toxicants. Chronic As poisoning through contaminated drinking water reportedly results in cardiovascular diseases, cancers and abnormalities in the nervous systems in biological organisms. One of the mechanisms underlying As-induced toxicity is oxidative stress, including formation of reactive oxygen species (ROS), and elevated lipid peroxidation (LP), which may result in cell death. In CNS, an acute As exposure in human may cause encephalopathy and chronic exposures of As produce cognitive deficits, distal axon degeneration and demyelination. In the present study, the effect of As on MPTP-induced neurotoxicity in CNS was investigated. 1-methyl-4-phenyl-1, 2, 3, 6-tetrapyridine (MPTP), a dopaminergic neurotoxin, is commonly used to degenerate dopaminergic neurons in the CNS. MPTP-induced neurotoxicity is reportedly mediated via inhibition of complex I in mitochondria, elevation in oxidative stress and energy depletion. Adult, male BALB/c mice were randomly divied into 4 groups, solvent+saline(control group)、solvent+MPTP(MPTP group)、As+saline(As group) and As+MPTP(As+MPTP group). Mice received daily oral administration of As (6 mg/kg) or solvent for 21 days and seven daily intraperitoneal injection of MPTP (20 mg/kg) or saline(0.2ml)for the last seven days. Neither MPTP, nor As, nor MPTP+As altered the body weight of mice. In vitro study showed that chronic MPTP or As alone did not change auto-oxidation or iron-induced lipid peroxidation of brain homogenates from MPTP- or As-treated mice. However, As pretreatment attenuated MPTP–induced elevation in auto-oxidation and iron-induced lipid peroxidation of brain homogenates. While MPTP depleted striatal dopamine content, systemic As did not alter striatal dopamine content. Nevertheless, MPTP-induced depletion in striatal dopamine content was potentiated when mice pretreated with As. Similar results were observed in that As augmented MPTP-induced reduction in tyrosine hydroxylase immunoreactivity by immunostaining. MPTP, As alone or MPTP+As did not change striatal GSH content and GPx activity. However, MPTP and As decreased catalase activity in the striatum. In addition, systemic As had no effect on Bcl-2, increased Bax expression and decreased Bcl-2/Bax ratio. However, As had no effect on MPTP-induced reduction in Bcl-2/Bax ratio in mouse striatum. Conclusively, As appears to potentiate MPTP-induced neurotoxicity in the nigrostriatal dopaminergic system in mice. However, GSH, GPx and Bcl-2 may not be involved in As-induced augmentation of MPTP-induced neurotoxicity.
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