Oxidative stress involves in astrocytic alterations induced by manganese

被引:103
作者
Chen, CJ [1 ]
Liao, SL [1 ]
机构
[1] Taichung Vet Gen Hosp, Dept Educ & Res, Taichung 40705, Taiwan
关键词
astrocyte; cytokine; manganese; manganism; metal; stellation;
D O I
10.1006/exnr.2002.7894
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It is hypothesized that manganese neurotoxicity could be secondary to a diminuition of cellular protective and scavenger mechanisms. Since manganese is known to be sequestered in glial cells, we investigated possible neurotoxic mechanisms involving astrocytes in vitro. Astrocytes differentiated into process-bearing stellate cells in response to manganese treatment. Manganese concentration dependently decreased cellular DNA synthesis, glial fibrillary acidic protein expression, energy production, antioxidant capacity, and glutamate transporter activity. In contrast, manganese increased glutamine synthetase protein expression and cytokine-stimulated interleukin 6 mRNA expression. Under the concentration of 0.1 mM manganese chloride caused no significant astrocyte death even up to 48 h after treatment. That is, these astrocytic alterations proceeded before the onset of cell demise. As a possible mediator of manganese-derived alterations, we determined intracellular redox state in astrocytes. Manganese time-dependently changed intracellular redox potential into oxidized state. The influx of manganese and its resultant oxidative stress was essential to most of the alterations, except for the action on stellation. Astrocytes are central component of the brain's antioxidant defense. Therefore, the observations suggest that dysfunction of astrocytes possibly involved in neurotoxic action of Manganese. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:216 / 225
页数:10
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