Farghali H, Martínek J, Masek K
Institute of Pharmacology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Methods Find Exp Clin Pharmacol. 1999 Jul-Aug;21(6):395-402. doi: 10.1358/mf.1999.21.6.541919.
S-nitroso-N-acetyl penicillamine (SNAP, 0.1-0.5 mM) caused release of nitric oxide (NO) into the perfusion medium of immobilized hepatocytes. Oxidative injury of hepatocytes was evoked by tert-butyl hydroperoxide (TBH, 1 mM) and the functional and morphological ultrastructural integrity of the cells was monitored. At the end of a 270-min perfusion period, SNAP-induced NO reduced lactate dehydrogenase leakage in TBH-injured hepatocytes as compared to untreated TBH-injured cells (122% +/- 5 vs. 146% +/- 6 of control levels), lipid peroxides production (2.7 +/- 0.2 vs. 3.7 +/- 0.3 nmol/10(6) cells), increased O2 consumption (26 +/- 2 vs. 12 +/- 1 nmol/10(6) cells) although urea synthesis was reduced. SNAP improved the formation of granules in the Golgi complex as compared to untreated TBH-injured hepatocytes and preserved the ultrastructural architecture of mitochondria and the smooth endoplasmic reticulum. The present data support a possible protective role of NO in oxidative liver injury.
S-亚硝基-N-乙酰青霉胺（SNAP，0.1 - 0.5 mM）可使一氧化氮（NO）释放到固定化肝细胞的灌注培养基中。叔丁基过氧化氢（TBH，1 mM）可引发肝细胞的氧化损伤，并监测细胞的功能和形态超微结构完整性。在270分钟的灌注期结束时，与未处理的TBH损伤细胞相比，SNAP诱导产生的NO可减少TBH损伤肝细胞中乳酸脱氢酶的泄漏（分别为对照水平的122% ± 5和146% ± 6），减少脂质过氧化物的产生（分别为2.7 ± 0.2和3.7 ± 0.3 nmol/10⁶个细胞），增加氧气消耗（分别为26 ± 2和12 ± 1 nmol/10⁶个细胞），尽管尿素合成减少。与未处理的TBH损伤肝细胞相比，SNAP可改善高尔基体中颗粒的形成，并保留线粒体和滑面内质网的超微结构。目前的数据支持NO在氧化型肝损伤中可能具有保护作用。
