Physiological functions of gangliosides and these applications

1)GM1对小鼠脾脏的剂量依赖性酶抑制我们以前的研究表明，体内给药外源性神经节苷脂可以调节大脑中的酶网络。在目前的研究中，我们测试了另一个器官--脾是否存在这种情况。通过对剂量效应关系的检验，发现GM1的酶促调节作用存在一个最佳剂量。虽然最适量因所检查的每种水解酶而异，但通常落在50克/公斤体重的范围内。这一发现使我们得出结论，神经节苷脂的酶调节作用不仅来自于substances.(Chem.Pharm.Bull.‘40,1958-1960,1992)2).Deficiency基因缺陷小鼠体内多个器官半乳糖苷酶活性的高分子外源GMZ的奇怪作用。为了了解这种异常与器官或细胞的一般代谢的关系，我们比较了WHT/Ht小鼠和对照组BALB/c小鼠以及不给予GM2和GM3的小鼠肝、脑、脾和肾中17种水解酶的活性。无论GM2或GM3处理，WHT/Ht小鼠所有受试器官的半乳糖苷酶活性均显著低于对照组。这种一致性与已知的神经节苷脂表达的器官依赖性异质性形成对比，从而表明在该模型动物中GM2缺陷与半乳糖苷酶缺陷是独立的。

1).Dose-dependent enzyme suppression in spleen induced by GM1 administration to miceOur previous studies suggested that the administration of exogenous gangliosides to the body modulates enzymatic networks in the brain. In the present study, we tested whether that is the case with another organ, spleen. By testing the dose response relationship, we found that there is a optimum dose for the effect of enzymatic modulation of GM1 administration. Although the optimum level varied depending on each of the examined hydrolytic enzymes, it usually fell in the range around 50 mug/kg body weight. The findings led us to conclude that the enzyme-modulating actions of gangliosides come not merely from the bizarre actions in vivo of high molecular exogegeous substances.(Chem.Pharm.Bull.'40,1958-1960,1992)2).Deficiency of galactosidase activity in multiple organs in GM2-deficient miceWHT/Ht mice are known to have GM2 deficiency especially in the liver. In order to known the relationship of this abnormality to the general metabolism in organs or cells, we compared 17 hydrolytic enzyme activities in the liver, brain, spleen, and kidney between the WHT/Ht mice and control BALB/c mice or without administration of GM2 and GM3. Regardless of the GM2 or GM3 treatment, the galactosidase activity was markedly low in all of the tested organs in the WHT/Ht mice when compared with that in the control animals. This consistency stands in contrast with the known organ-dependency heterogeneity of ganglioside expression and thus indicates independency of the GM2 deficiency from the galactosidase deficiency in this model animal.(J.Clin.Biochem.Nutr., 13,189-197,1992)