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新生小鼠培养脑细胞中半乳糖的利用

Utilization of galactose in cultured brain cells of neonatal mice.

作者信息

Schwarz H P, Gennari K, Siegrist H P, Zuppinger K, Schäfer T, Wiesmann U, Herschkowitz N

出版信息

Pediatr Res. 1985 Jan;19(1):52-7. doi: 10.1203/00006450-198501000-00014.

Abstract

Metabolism of galactose was examined in dissociated brain cells from neonatal mice after 10-13 days in culture. Consumption of galactose at levels up to 26 mM was much less than consumption of glucose at corresponding concentrations. Lactate was consumed from the media at all galactose levels, in contrast to experiments with glucose in which lactate was formed and released into the media. Generation of CO2 from 4 mM glucose was 9-fold greater than from an equimolar level of galactose. Relatively low concentrations of glucose could reduce uptake of galactose, whereas galactose at levels up to 11.6 mM failed to inhibit consumption of glucose or formation of lactate. In glucose-deficient states, galactose supplementation of the media led to a marked increase in sulfatide synthesis by oligodendrocytes in the culture with a maximum effect at 2.3 mM. Under these conditions, [1-14C]galactose was incorporated directly into the carbohydrate portion of sulfatide, although most of the label was found in phospholipids and in the nonlipid fraction of the cellular homogenate. These data suggest that galactose is poorly metabolized by brain cells, but does not exhibit toxic effects.

摘要

在培养10 - 13天后,对新生小鼠分离的脑细胞中的半乳糖代谢进行了检测。在高达26 mM的浓度下,半乳糖的消耗量远低于相应浓度下葡萄糖的消耗量。与葡萄糖实验中乳酸生成并释放到培养基中不同,在所有半乳糖水平下,培养基中的乳酸都被消耗。4 mM葡萄糖产生的二氧化碳比等摩尔水平的半乳糖多9倍。相对低浓度的葡萄糖可减少半乳糖的摄取,而高达11.6 mM的半乳糖未能抑制葡萄糖的消耗或乳酸的形成。在葡萄糖缺乏状态下,向培养基中添加半乳糖会导致培养物中少突胶质细胞的硫脂合成显著增加,在2.3 mM时效果最佳。在这些条件下,[1 - 14C]半乳糖直接掺入硫脂的碳水化合物部分,尽管大部分标记物存在于磷脂和细胞匀浆的非脂质部分中。这些数据表明,脑细胞对半乳糖的代谢能力较差,但未表现出毒性作用。

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