The presence of calbindin in rat cortical neurons protects in vitro from oxydative stress

被引:35
作者
Hugon, J
Hugon, F
Esclaire, F
Lesort, M
Diop, AG
机构
[1] Cellular Neurobiology Unit, Laboratory of Histology, Faculty of Medicine, 87025 Limoges Cédex
关键词
neuronal culture; oxydative stress; calbindin D-28K; neurodegeneration;
D O I
10.1016/0006-8993(95)01393-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Free radicals are highly reactive chemicals containing an unpaired electron and are normally produced by the cellular metabolism. The oxydative stress is defined as a lack of balance between the production of free radicals and the activity of antioxydant metabolites. It induces cellular damages to lipids, proteins and membranes. Abnormal calcium metabolism can be a consequence of oxydative stress leading to increased intracellular concentrations. Calbindin D28K is a calcium binding protein which could have a neuroprotective action against various cellular insults. In this study rat cortical cell cultures were exposed during various times and at different concentrations to the couple Xanthine/Xanthine oxydase (XA/XO), which produces the superoxyde radical O-2(_). Neuronal survival revealed that XA/XO is toxic for cortical cell cultures. The Calbindin D-28k immunocytochemical study shows that the percentages of Calbindin positive cells are greater in surviving neurons following the XA/XO exposure compared to controls. There is a time-dependent and a dose-dependent relation between the number of surviving neurons and the percentage of Calbindin positive neurons. These results suggest that the presence of cytosolic neuronal Calbindin D-28k is associated with a greater resistance to oxydative stress.
引用
收藏
页码:288 / 292
页数:5
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