Inhibition of NADPH supply by 6-aminonicotinamide: effect on glutathione, nitric oxide and superoxide in J774 cells
Inhibition of NADPH supply by 6-aminonicotinamide: effect on glutathione, nitric oxide and superoxide in J774 cells
复制标题
DOI：
10.1016/s0014-5793(98)00959-4
复制
发表时间：
1998-08-28
期刊：
影响因子：
3.5
通讯作者：
Noronha-Dutra, AA
中科院分区：
文献类型：
--
作者：
Hothersall, JS;Gordge, M;Noronha-Dutra, AA
我们已经研究了J774细胞的一氧化氮（NO）的生产和谷胱甘肽的维护的完整性，而NADPH的供应受到损害的戊糖途径与6-氨基烟酰胺的抑制。在静息细胞中，6-磷酸葡萄糖酸积累开始后4小时和谷胱甘肽耗尽后24小时的6-氨基烟酰胺治疗。脂多糖/干扰素-λ激活细胞后，谷胱甘肽含量降低约50%，而6-氨基烟酰胺处理则使谷胱甘肽含量增加至对照组的31.2%（P < 0.05）。6-氨基烟酰胺可抑制激活细胞中NO的产生60%（P < 0.01），抑制酵母多糖激活细胞中超氧化物的产生50%（P < 0.01）。因此，通过戊糖途径产生NADPH对于维持巨噬细胞NO产生同时维持谷胱甘肽的保护水平是重要的。(C)1998年欧洲生物化学学会联合会。
We have examined the integrity of J774 cell nitric oxide (NO) production and glutathione maintenance, whilst NADPH supply was compromised by inhibition of the pentose pathway with 6-aminonicotinamide. In resting cells 6-phosphogluconate accumulation began after 4 h and glutathione depletion after 24 h of 6-aminonicotinamide treatment. Cellular activation by lipopolysaccharide/interferon-lambda decreased glutathione by similar to 50% and synchronous 6-aminonicotinamide treatment exacerbated this to 31.2% of control (P < 0.05), In activated cells NO, production was inhibited by 60% with 6-aminonicotinamide (P < 0.01), and superoxide production by 50% (P < 0.01) in zymosan-activated cells. NADPH production via the pentose pathway is therefore important to sustain macrophage NO production whilst maintaining protective levels of glutathione. (C) 1998 Federation of European Biochemical Societies.