Suppr超能文献

氮耗竭导致粟酒裂殖酵母中谷胱甘肽含量和γ-谷氨酰转肽酶上调。

Nitrogen depletion causes up-regulation of glutathione content and gamma-glutamyltranspeptidase in Schizosaccharomyces pombe.

作者信息

Song Seung-Hyun, Lim Chang-Jin

机构信息

Division of Life Sciences and Research Institute of Life Sciences, Kangwon National University, Chuncheon 200-701, Republic of Korea.

出版信息

J Microbiol. 2008 Feb;46(1):70-4. doi: 10.1007/s12275-007-0244-y.

Abstract

This work aims to elucidate the relationship between nitrogen depletion and Glutathione (GSH) level in Schizosaccharomyces pombe. The total GSH level was much higher in the Pap1-positive KP1 cells than in the Pap1-negative TP108-3C cells, suggesting that synthesis of GSH is dependent on Pap1. When the Pap1-positive KP1 cells were transferred to the nitrogen-depleted medium, total GSH level significantly increased up to 6 h and then slightly declined after 9 h. Elevation of the total GSH level was observed to be much less with the Pap1-negative cells. However, glucose deprivation was not able to enhance the GSH level in the KP1 cells. Activity of gamma-glutamyltranspeptidase (gamma-GT), an enzyme in the first step of GSH catabolism, also increased during nitrogen depletion. The total GSH level was more significantly enhanced in the KP1 cells overexpressing gamma-GT2 than gamma-GT1 during nitrogen starvation. Reactive oxygen species (ROS) levels were not changed during nitrogen starvation in both Pap1-positive and Pap1-negative cells. Collectively, nitrogen depletion causes up-regulation of GSH synthesis and gamma-GT in a Pap1-dependent manner.

摘要

这项工作旨在阐明粟酒裂殖酵母中氮消耗与谷胱甘肽(GSH)水平之间的关系。Pap1阳性的KP1细胞中的总GSH水平远高于Pap1阴性的TP108-3C细胞,这表明GSH的合成依赖于Pap1。当Pap1阳性的KP1细胞转移到氮耗尽的培养基中时,总GSH水平在6小时内显著增加,然后在9小时后略有下降。在Pap1阴性细胞中,总GSH水平的升高要少得多。然而,葡萄糖剥夺并不能提高KP1细胞中的GSH水平。γ-谷氨酰转肽酶(γ-GT)是GSH分解代谢第一步中的一种酶,其活性在氮消耗期间也会增加。在氮饥饿期间,过表达γ-GT2的KP1细胞中的总GSH水平比过表达γ-GT1的细胞更显著地升高。在Pap1阳性和Pap1阴性细胞的氮饥饿期间,活性氧(ROS)水平均未发生变化。总的来说,氮消耗以Pap1依赖的方式导致GSH合成和γ-GT的上调。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验