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  2. College of Health Care and Management/健康管理學院
  3. School of Occupational Safety and Health/職業安全衛生學系
  4. 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
 
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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

Date Issued
2015
Author(s)
鐘耀邦
Yao-Pang Chung
Advisor
巖正傑
URI
https://handle.ncl.edu.tw/11296/e2jdrv
https://scholars.csmu.edu.tw/handle/123456789/20412
Abstract
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
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
Subjects
甲基汞
神經毒性
細胞凋亡
內質網壓力
AKT蛋白
活性氧物種
Methylmercury
Neurotoxicity
Apoptosis
endoplasmic reticulum stress
Akt
reactive oxygen species
Type
thesis
File(s)
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103CSMU5590008-001.zip

Size

3.2 MB

Format

Unknown

Checksum

(MD5):eddcbd018e52707468a0728e2a302210

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