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蛋氨酸亚砜亚胺致痫性啮齿动物脑内糖原合成及果糖-1,6-二磷酸酶的免疫细胞化学研究

Glycogen synthesis and immunocytochemical study of fructose-1,6-biphosphatase in methionine sulfoximine epileptogenic rodent brain.

作者信息

Hevor T K, Delorme P, Beauvillain J C

出版信息

J Cereb Blood Flow Metab. 1986 Jun;6(3):292-7. doi: 10.1038/jcbfm.1986.51.

DOI:10.1038/jcbfm.1986.51
PMID:3011827
Abstract

The effects of the convulsant methionine sulfoximine (MSO) on the glucose pathway have been investigated in mouse and rat brain. The key gluconeogenic enzyme fructose-1,6-biphosphatase (FBPase) (EC 3.1.3.11) was immunostained by rat anti-FBPase antibody. The rat cortex slices were very lightly stained, almost unstained in controls. After MSO injection, there was a marked staining only in astrocytes (perikarya, processes, and end feet). The activity of this enzyme also increased. MSO induced an increase of 63% in the stability at heating (47 degrees C) and of 36% in the stability at proteolysis (trypsin, 10 micrograms/ml) of FBPase. The convulsant had no effect on the concentrations of the metabolites related to the FBPase-phosphofructokinase step, i.e., fructose-1,6-biphosphate, glyceraldehyde-3-phosphate, and dihydroxyacetone phosphate, before, during, or after the convulsions. These results show that the cellular site of glucose pathway impairment induced by MSO in rodent brain is presumably the astroglial cells and that one mechanism of glycogenesis could be the reinforcement of the molecules of FBPase, which enhances gluconeogenesis. A hypothetical diagram of glucose metabolism under the effect of MSO has been proposed.

摘要

已在小鼠和大鼠脑中研究了惊厥剂蛋氨酸亚砜亚胺(MSO)对葡萄糖代谢途径的影响。用大鼠抗果糖-1,6-二磷酸酶(FBPase)抗体对关键的糖异生酶果糖-1,6-二磷酸酶(FBPase)(EC 3.1.3.11)进行免疫染色。大鼠皮质切片染色很浅,对照组几乎未染色。注射MSO后,仅在星形胶质细胞(胞体、突起和终足)中有明显染色。该酶的活性也增加。MSO使FBPase在加热(47℃)时的稳定性增加63%,在蛋白水解(胰蛋白酶,10微克/毫升)时的稳定性增加36%。惊厥剂在惊厥前、惊厥期间或惊厥后对与FBPase-磷酸果糖激酶步骤相关的代谢物浓度,即果糖-1,6-二磷酸、3-磷酸甘油醛和磷酸二羟丙酮,没有影响。这些结果表明,MSO在啮齿动物脑中诱导的葡萄糖代谢途径损伤的细胞部位可能是星形胶质细胞,并且糖原生成的一种机制可能是增强FBPase分子,从而增强糖异生。已提出了一个在MSO作用下葡萄糖代谢的假想图。

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