Methylmercury Induces Pancreatic -Cell Apoptosis and Dysfunction
详细信息 查看全文
- 作者：Ya Wen Chen ; Chun Fa Huang ; Keh Sung Tsai ; Rong Sen Yang ; Cheng Chieh Yen ; Ching Yao Yang ; Shoei Yn Lin-Shiau ; Shing Hwa Liu
- 刊名：Chemical Research in Toxicology
- 出版年：2006
- 出版时间：August 2006
- 年：2006
- 卷：19
- 期：8
- 页码：1080 - 1085
- 全文大小：241K
- 年卷期：v.19,no.8(August 2006)
- ISSN：1520-5010
文摘
Mercury is a well-known toxic metal, which induces oxidative stress. Pancreatic 
-cells are vulnerableto oxidative stress. The pathophysiological effect of mercury on the function of pancreatic -cells remainsunclear. The present study was designed to investigate the effects of methylmercury (MeHg)-inducedoxidative stress on the cell viability and function of pancreatic -cells. The number of viable cells wasreduced 24 h after MeHg treatment in a dose-dependent manner with a range from 1 to 20 
M. 2',7'-Dichlorofluorescein fluorescence as an indicator of reactive oxygen species (ROS) formation after exposureof HIT-T15 cells or isolated mouse pancreatic islets to MeHg significantly increased ROS levels. MeHgcould also suppress insulin secretion in HIT-T15 cells and isolated mouse pancreatic islets. After 24 hof exposure to MeHg, HIT-T15 cells had a significant increase in mercury levels with a dose-dependentmanner. Moreover, MeHg displayed several features of cell apoptosis including an increase of the sub-G1 population and annexin-V binding. Treatment of HIT-T15 cells with MeHg resulted in disruption ofthe mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytosoland activation of caspase-3. Antioxidant N-acetylcysteine effectively reversed the MeHg-induced cellularresponses. Altogether, our data clearly indicate that MeHg-induced oxidative stress causes pancreatic-cell apoptosis and dysfunction.
-cells are vulnerableto oxidative stress. The pathophysiological effect of mercury on the function of pancreatic -cells remainsunclear. The present study was designed to investigate the effects of methylmercury (MeHg)-inducedoxidative stress on the cell viability and function of pancreatic -cells. The number of viable cells wasreduced 24 h after MeHg treatment in a dose-dependent manner with a range from 1 to 20 M. 2',7'-Dichlorofluorescein fluorescence as an indicator of reactive oxygen species (ROS) formation after exposureof HIT-T15 cells or isolated mouse pancreatic islets to MeHg significantly increased ROS levels. MeHgcould also suppress insulin secretion in HIT-T15 cells and isolated mouse pancreatic islets. After 24 hof exposure to MeHg, HIT-T15 cells had a significant increase in mercury levels with a dose-dependentmanner. Moreover, MeHg displayed several features of cell apoptosis including an increase of the sub-G1 population and annexin-V binding. Treatment of HIT-T15 cells with MeHg resulted in disruption ofthe mitochondrial membrane potential and release of cytochrome c from the mitochondria to the cytosoland activation of caspase-3. Antioxidant N-acetylcysteine effectively reversed the MeHg-induced cellularresponses. Altogether, our data clearly indicate that MeHg-induced oxidative stress causes pancreatic-cell apoptosis and dysfunction.