慢性有机汞中毒的猴、兔和人脑神经节苷脂及其他脂质的异常。
Abnormalities in gangliosides and other lipids of monkey, rabbit and human brains with chronic organic mercury intoxication.
作者信息
Ando S, Toyoda Y, Nagai Y, Ikuta F
出版信息
Jpn J Exp Med. 1985 Feb;55(1):1-6.
The distribution patterns of gangliosides and other major lipids in the monkey, rabbit and human brains with chronic organic mercury intoxication were examined. Various areas of the monkey brains were tested for alterations in the lipid composition in detail. Phosphatidylethanolamine and phosphatidylcholine slightly decreased, and sphingomyelin increased in all the areas tested of the intoxicated brains. The total ganglioside concentration was elevated in the frontal and basal ganglia gray matter tissues. In the percentage distribution of gangliosides, GD1b, GT1b and GQ1b (B pathway, [19, 20]) increased, while GM2, GM1 and GD1a (A pathway, [19, 20]) decreased. Similar ganglioside pattern changes were observed also in a human brain and in a rabbit brain with chronic organic mercury intoxication. The altered distribution patterns of gangliosides may be attributable to the proliferation of reactive astrocytes due to organic mercury.
研究了慢性有机汞中毒的猴子、兔子和人类大脑中神经节苷脂及其他主要脂质的分布模式。对猴子大脑的各个区域进行了详细的脂质成分变化测试。在中毒大脑的所有测试区域中，磷脂酰乙醇胺和磷脂酰胆碱略有下降，而鞘磷脂增加。额叶和基底神经节灰质组织中的总神经节苷脂浓度升高。在神经节苷脂的百分比分布中，GD1b、GT1b和GQ1b（B途径，[19,20]）增加，而GM2、GM1和GD1a（A途径，[19,20]）减少。在慢性有机汞中毒的人类大脑和兔子大脑中也观察到了类似的神经节苷脂模式变化。神经节苷脂分布模式的改变可能归因于有机汞导致的反应性星形胶质细胞增殖。
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