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磷酸己糖途径抑制后C-1300神经母细胞瘤细胞中的葡萄糖代谢

Glucose metabolism in C-1300 neuroblastoma cells after inhibition of hexose monophosphate pathway.

作者信息

Kolbe H, Keller K, Lange K, Herken H

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1977 Jan;296(2):123-30. doi: 10.1007/BF00508463.

Abstract
  1. Application of 6-AN (0.01 mg/ml) leads to a strong accumulation of 6-PG in C-1300 neuroblastoma cells which, however, only amounts to one third of that found in C-6 glial cells. 2. In C-1300 neuroblastoma cells dephosphorylation of the accumulated 6-PG causes a rise of the intracellular gluconate to eight times the value found for 6-PG. It is four times higher than the gluconate content observed in C-6 glial cells. 3. Although 6-PG is a competitive inhibitor of PGI it causes no reduction of glycolytic flux and ATP content in stationary phase C-1300 neuroblastoma cells in contrast to the strong reduction of glycolytic flux and ATP content observed in C-glial cells. 4. The intracellular Glc-6-P and Fru-6-P content of C-1300 neuroblastoma cells increases by four to five times after treatment with 6-AN. Both this increase and the decrease of Fru-1,6-P2 content point to an inhibition of the phosphofructokinase. 5. In contrast to C-6 glial cells no morphological changes could be observed in C-1300 neuroblastoma cells up to 24 h after administration of 6-AN.
摘要
  1. 应用6-氨基烟酰胺(0.01毫克/毫升)会导致C-1300神经母细胞瘤细胞中6-磷酸葡萄糖酸(6-PG)大量积累,然而,其积累量仅为C-6神经胶质细胞中积累量的三分之一。2. 在C-1300神经母细胞瘤细胞中,积累的6-PG去磷酸化会使细胞内葡萄糖酸盐升高至6-PG所测值的八倍。它比C-6神经胶质细胞中观察到的葡萄糖酸盐含量高四倍。3. 尽管6-PG是磷酸葡萄糖异构酶(PGI)的竞争性抑制剂,但与在C-神经胶质细胞中观察到的糖酵解通量和ATP含量的强烈降低相反,它不会导致静止期C-1300神经母细胞瘤细胞的糖酵解通量和ATP含量降低。4. 用6-氨基烟酰胺处理后,C-1300神经母细胞瘤细胞内的6-磷酸葡萄糖(Glc-6-P)和6-磷酸果糖(Fru-6-P)含量增加四到五倍。这种增加以及1,6-二磷酸果糖(Fru-1,6-P2)含量的降低均表明磷酸果糖激酶受到抑制。5. 与C-6神经胶质细胞不同,在给予6-氨基烟酰胺后长达24小时,未观察到C-1300神经母细胞瘤细胞有形态变化。

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