Amin N, Pearce B
Pharmacology Department, The School of Pharmacy, London, UK.
Brain Res. 1997 Oct 31;773(1-2):227-30. doi: 10.1016/s0006-8993(97)00955-4.
The exposure of cultured astrocytes to peroxynitrite (ONOO-) for 40 min resulted in a concentration-dependent increase in the release of lactate dehydrogenase from the cells into the bathing medium over the following 24 h. Control experiments showed that the breakdown products of ONOO- contribute, to some extent, to its ability to cause cell death but that the drug vehicle (0.3 M NaOH), which increased the pH of the bathing medium to 9.4, had little effect. The cytotoxic action of ONOO- was mimicked by 3-morpholinosydnonimine (SIN-1) which liberates both nitric oxide (NO) and superoxide but not by S-nitrosoglutathione which liberates only NO. SIN-1-induced cytotoxicity was reversed in a concentration-dependent manner by superoxide dismutase and attenuated by haemoglobin suggesting that the effect of SIN-1 is due, at least in part, to the formation of ONOO-.
将培养的星形胶质细胞暴露于过氧亚硝酸盐（ONOO-）40分钟后，在接下来的24小时内，细胞内乳酸脱氢酶释放到培养液中的量呈浓度依赖性增加。对照实验表明，ONOO-的分解产物在一定程度上导致了细胞死亡，而将培养液pH值提高到9.4的药物载体（0.3 M NaOH）几乎没有影响。3-吗啉代辛二酮（SIN-1）可模拟ONOO-的细胞毒性作用，SIN-1可释放一氧化氮（NO）和超氧化物，但仅释放NO的S-亚硝基谷胱甘肽则无此作用。超氧化物歧化酶可浓度依赖性地逆转SIN-1诱导的细胞毒性，血红蛋白可减弱该毒性，这表明SIN-1的作用至少部分归因于ONOO-的形成。
