甲基汞透過內質網壓力調控細胞凋亡及誘發神經元細胞死亡:其中以活性氧物種抑制AKT蛋白活化扮演關鍵角色

Methylmercury induces neuronal cell death through an endoplasmic reticulum regulated apoptosis pathway: The role of reactive oxygen species-mediated Akt inactivation

鐘耀邦(Yao-Pang Chung)

指導教授 ： 巖正傑

中山醫學大學/健康管理學院/職業安全衛生學系碩士班/碩士(2015年)

https://doi.org/10.6834/CSMU.2015.00100

摘要

甲基汞(Methylmercury, MeHg)是眾所周知的環境汙染物質，人類藉由食用海洋魚類動物間接暴露甲基汞，在流行病學調查研究中發現在污染區中人體內血液含有累積的汞(> 40

關鍵字

甲基汞 ； 神經毒性 ； 細胞凋亡 ； 內質網壓力 ； AKT蛋白 ； 活性氧物種

並列摘要

Epidemiological studies have positively linked mercury exposure and neurodegenerative diseases. Methylmercury (MeHg), an organic form of mercury, is highly ubiquitous environmental toxicant and a well-known human neurotoxic agent that easily crosses the blood-brain barrier and causes irreversible injury in the central nervous system (CNS). However, the molecular mechanisms underlying MeHg-induced neurotoxicity remain unknown. Here, the present study found that Neuro-2a cells underwent apoptosis in response to MeHg (1-5

並列關鍵字

Methylmercury ； Neurotoxicity ； Apoptosis ； endoplasmic reticulum stress ； Akt ； reactive oxygen species

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