Grant R S, Kapoor V
School of Physiology and Pharmacology, Faculty of Medicine, University of New South Wales, Sydney, Australia.
J Neurochem. 1998 Apr;70(4):1759-63. doi: 10.1046/j.1471-4159.1998.70041759.x.
The potential for regeneration of intracellular pyridine nucleotide levels from different precursors, after peroxide-induced NAD depletion, in cultured glial cells was investigated. Cultured murine glial cells showed a decrease in intracellular NAD levels of >40% after treatment with H2O2 (100 microM). Removal of the H2O2 followed by a 2-h incubation did not result in NAD recovery in the absence of precursors. However, NAD levels increased significantly in these cells after the following substrate additions, at minimum effective concentrations of 1 mM for quinolinic acid (QUIN), 500 microM for nicotinamide, and 2 microM for nicotinic acid. The regeneration of significant amounts of NAD from nicotinic acid at doses 250 and 500 times lower than either nicotinamide or QUIN indicates a preferred route for NAD biosynthesis in glial cells in vitro, probably via nicotinic acid phosphoribosylation.
研究了在培养的神经胶质细胞中，过氧化物诱导NAD耗竭后，不同前体物质使细胞内吡啶核苷酸水平再生的潜力。用H2O2（100微摩尔）处理后，培养的小鼠神经胶质细胞内NAD水平降低了40%以上。在没有前体物质的情况下，去除H2O2并孵育2小时后，NAD水平并未恢复。然而，在添加以下底物后，这些细胞中的NAD水平显著增加，喹啉酸（QUIN）的最低有效浓度为1毫摩尔，烟酰胺为500微摩尔，烟酸为2微摩尔。与烟酰胺或QUIN相比，剂量低250倍和500倍的烟酸能大量再生NAD，这表明体外神经胶质细胞中NAD生物合成的首选途径可能是通过烟酸磷酸核糖基化。
