Oberle S, Schröder H
Department of Pharmacology and Toxicology, School of Pharmacy, Martin Luther University, Halle (Saale), Germany.
Nitric Oxide. 1997 Aug;1(4):308-14. doi: 10.1006/niox.1997.0132.
In porcine aortic endothelial cells, a 20-h incubation with hydrogen peroxide (0.5 mM) markedly reduced the number of viable cells. A 6-h preincubation with linsidomine (SIN-1, 0.5 mM) protected endothelial cells from hydrogen peroxide-dependent cytotoxicity and increased the surviving endothelial cell fraction by 85%. This protection was associated with a 2.5-fold induction of ferritin heavy chain mRNA and ferritin protein by SIN-1. The nitric oxide donor glyceryl trinitrate was also found to induce transcriptional and translational expression of ferritin heavy chain. A protective effect comparable to SIN-1 was observed when preincubating the cells with iron-free apoferritin (1 mg/ml). These findings suggest that ferritin induction, presumably via release of nitric oxide, may be a mechanism underlying long-term cytoprotection by SIN-1 against oxidative stress.
在猪主动脉内皮细胞中，用过氧化氢（0.5 mM）孵育20小时可显著减少活细胞数量。用亚硝基铁氰化钠（SIN-1，0.5 mM）预孵育6小时可保护内皮细胞免受过氧化氢依赖性细胞毒性，并使存活的内皮细胞比例增加85%。这种保护作用与SIN-1诱导铁蛋白重链mRNA和铁蛋白蛋白增加2.5倍有关。还发现一氧化氮供体硝酸甘油可诱导铁蛋白重链的转录和翻译表达。当用无铁脱铁铁蛋白（1 mg/ml）预孵育细胞时，观察到与SIN-1相当的保护作用。这些发现表明，推测通过一氧化氮释放诱导铁蛋白可能是SIN-1对氧化应激进行长期细胞保护的潜在机制。
