Protein binding of NADH on chemical preconditioning
Protein binding of NADH on chemical preconditioning
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DOI：
10.1046/j.1471-4159.2000.0750329.x
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发表时间：
2000-07-01
影响因子：
4.7
通讯作者：
Riepe, MW
中科院分区：
文献类型：
--
作者：
Huber, R;Büchner, M;Riepe, MW
化学预适应是近年来提出的一种新的神经保护策略，其机制尚不清楚，可在低氧状态下维持能量代谢。NADH含量的缺氧性增加可被预适应所减弱。本研究的目的是调查缺氧性NADH增加的减弱是否是由于游离NADH和蛋白质结合NADH之间的转换。NADH在溶液中的最大荧光波长为469.2 nm。在未经处理的小鼠海马片中，在CA1(平均值+/-SD；p<；0.01vs.溶液)和454.6+/-6.1 nm(p<；0.01vs.溶液)中，lambda(对照起始)为456.2+/-5.3nm.CA3[p<；0.01vs.溶液，(NS)对lambda(对照起始)无显著意义]。在用20 mg/kg 3-硝基丙酸体内处理的动物的切片中，CA1和CA3的Lambda(预适应开始)分别为439.2+/-5.0 nm(p<；0.001比对照)和434.2+/-6.4 nm(p<；0.001比对照；NS到lambda(预适应)(在CA1开始))。在对照组中，CA1和CA3的荧光最大值分别移动到458.2+/-1.3 nm和456.0+/-3.6nm.在3-硝基丙酸预适应条件下，CA1(P<；0.03vs.Start)和CA3(P<；0.03vs.Start)的低氧预适应波长分别移动到446.4+/-4.3nM和438.6+/-6.9nm.预适应后，游离和蛋白质结合的NADH的后氧性衰退减少，我们得出结论，化学预适应提高了缺氧耐受性，从而降低了游离NADH的水平。在低氧预适应后，游离NADH含量的减少保持不变。
Chemical preconditioning, an emerging neuroprotective strategy described in recent years, results in preserved energy metabolism during hypoxia via yet unknown mechanisms. The hypoxic increase of NADH content is attenuated by preconditioning. The goal of the present study was to investigate whether attenuation of the hypoxic NADH increase is due to a shift between free and protein-bound NADH. NADH in solution has a fluorescence maximum at 469.2 nm. In untreated mouse hippocampal slices, lambda(control onset) is 456.2 +/- 5.3 nm in CA1 (mean +/- SD; p < 0.01 vs. solution) and 454.6 +/- 6.1 nm in CA3 [p < 0.01 vs. solution, not significant (NS) to lambda(control onset) in CA1]. In slices prepared from animals pretreated in vivo with 20 mg/kg 3-nitropropionate, lambda(preconditioning onset) is 439.2 +/- 5.0 nm (p < 0.001 vs. control) in CA1 and 434.2 +/- 6.4 nm in CA3 (p < 0.001 vs. control; NS to lambda(preconditioning) (onset) in CA1). In controls, the fluorescence maximum shifts to lambda(control hypoxia) 458.2 +/- 1.3 nm in CA1 (NS vs. onset) and 456.0 +/- 3.6 nm in CA3 (NS vs, onset). On preconditioning with 3-nitropropionate, lambda(preconditioning hypoxia) shifts to 446.4 +/- 4.3 nm in CA1 (p < 0.03 vs. onset) and 438.6 +/- 6.9 nm in CA3 (p < 0.03 vs. onset). Posthypoxic decay of free and protein-bound NADH is diminished after preconditioning, We conclude that the free NADH level is reduced on an increase of hypoxic tolerance by chemical preconditioning. Reduction of free NADH content is maintained during hypoxia after preconditioning.