Deloncle R, Guillard O, Huguet F, Clanet F
Laboratoire de Chimie Bio-Inorganique, Faculté de Pharmacie, Tours, France.
Biol Trace Elem Res. 1995 Jan-Mar;47(1-3):227-33. doi: 10.1007/BF02790121.
The authors have used an experimental rat model of chronic aluminum (Al) intoxication to reproduce pathological signs analogous to those observed in humans for Alzheimer's disease or dialysis encephalopathy. Preliminary chronic intoxication was achieved during 5 wk by daily subcutaneous injection of a suspension of glutamate and Al prior to intravenous (i.v.) administration of sodium L-glutamate and Al chloride. A significant increase in Al content was observed in different areas of the brain, such as the hippocampus, the occipito-parietal cortex, the cerebellum, and the striatum. Moreover, half of the animals subcutaneously treated with Al glutamate had neurological disturbances, such as trembling, equilibrium difficulties, and convulsions leading to death about 1 h after i.v. administration. A significant increase in glutamic acid at the level of the occipito-parietal cortex was found in comparison with controls, which received only sodium L-glutamate or saline solution. These results show that the Al-L-glutamate complex may well induce a modification of the blood-brain barrier.
作者使用了慢性铝（Al）中毒的实验大鼠模型，以重现类似于人类阿尔茨海默病或透析性脑病中观察到的病理体征。在静脉注射L-谷氨酸钠和氯化铝之前，通过每日皮下注射谷氨酸和铝的悬浮液，在5周内实现了初步的慢性中毒。在大脑的不同区域，如海马体、枕顶叶皮质、小脑和纹状体中，观察到铝含量显著增加。此外，皮下注射谷氨酸铝的动物中有一半出现神经功能障碍，如颤抖、平衡困难和惊厥，静脉注射后约1小时导致死亡。与仅接受L-谷氨酸钠或盐溶液的对照组相比，在枕顶叶皮质水平发现谷氨酸显著增加。这些结果表明，铝-L-谷氨酸复合物很可能会引起血脑屏障的改变。
