Primed pentose cycle activity supports production and elimination of superoxide anion in Kupffer cells from rats treated with endotoxin in vivo.
Primed pentose cycle activity supports production and elimination of superoxide anion in Kupffer cells from rats treated with endotoxin in vivo.
复制标题
启动的戊糖循环活性支持体内用内毒素处理的大鼠库普弗细胞中超氧阴离子的产生和消除。
DOI：
10.1016/0167-4889(93)90134-b
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Spitzer,JJ
中科院分区：
文献类型：
--
作者：
Spolarics,Z;Bautista,AP;Spitzer,JJ
Glucose use and pentose cycle activity were determined in freshly isolated rat Kupffer cells 3 h after an iv injection of Escherichia coli endotoxin (0.1 mg/kg body weight), by using [1-14 C],[6-14 C] and [2-3 H] glucose. Endotoxin treatment in vivo caused a 5-fold increase in the basal glucose uptake in Kupffer cells. Pentose cycle activity was elevated from 8.7 to 13.6 nmol/h per 10 7 cells after endotoxin. In vitro treatment of the cells from saline-and endotoxin-treated animals with phorbol ester (10− 6 M) increased pentose cycle activity 2-fold and 8-fold, respectively. Phorbol ester caused a 50% increase in glucose uptake in both groups. t-Butyl hydroperoxide (0.5 mM) caused a similar increase in pentose cycle activity as phorbol ester. Glucose oxidation in the Krebs cycle was also doubled after endotoxin. KC from endotoxin-treated animals produced O− 2 spontaneously, and were primed to produce additional large amounts of O− 2 upon phorbol ester treatment. Addition of t-butyl hydroperoxide inhibited O− 2 production by Kupffer cells. Depletion of glutathione by N-ethylmaleimide (0.1 mM), or inhibition of NADPH oxidase by diphenyliodonium (0.1 mM) inhibited both the pentose cycle activity and the O− 2 production. Increasing the concentration of exogenous glucose in the cell medium elevated the glycolytic rate, while pentose cycle flux was not affected either under basal conditions or following subsequent challenges by phorbol ester or t-butyl hydroperoxide. Our data suggest that the endotoxin-induced elevated glucose use in Kupffer cells is accompanied by a primed state of the pentose cycle. This condition supports superoxide and macromolecule synthesis and could also represent a potentiated protective mechanism against oxidative cellular injury during bacterial infections.
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控制大鼠肝脏和其他组织中磷酸戊糖循环氧化阶段的辅因子的纯化和表征。
DOI：
10.1016/s0304-4165(89)80012-1
发表时间：
1989
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
G. García;M. Nogueira;M. Freire
通讯作者：
M. Freire
内毒素施用后不同器官对葡萄糖消耗增加的贡献。
影响因子：
4.8
作者：
K. Mészáros;C. Lang;G. Bagby;J. Spitzer
通讯作者：
J. Spitzer
输注肿瘤坏死因子后库普弗细胞中葡萄糖代谢上调。
影响因子：
4.1
作者：
Z. Spolarics;G. Bagby;C. Lang;J. Spitzer
通讯作者：
J. Spitzer
肝非实质细胞和白细胞对粒细胞巨噬细胞集落刺激因子的体内代谢反应
影响因子：
5.5
作者：
Z. Spolarics;Á. Schuler;G. Bagby;C. Lang;S. Nelson;J. Spitzer
通讯作者：
J. Spitzer
影响因子：
4.1
作者：
EGGLESTON, LV;KREBS, HA
通讯作者：
KREBS, HA