Wei T, Chen C, Zhao B, Xin W, Mori A
Institute of Biophysics, Academia Sinica, Beijing, China.
Biochem Mol Biol Int. 1998 Sep;46(1):89-97. doi: 10.1080/15216549800203592.
Apoptosis induced by peroxynitrite in cultured cerebellar granule cells was confirmed morphologically by chromatin condensation and biochemically by DNA laddering. A 30 min exposure to peroxynitrite (10 microM) initiated oxidative stress, which caused the formation of thiobarbituric acid-reactive substances (TBARS) and the alteration of cell membrane fluidity. Peroxynitrite treatment also caused ATP decrease and thus activated the apoptotic program. Pre-treating cells with antioxidant EPC-K1 (L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H -1- benzopyran-6-yl-hydrogen phosphate] potasium salt), a new water-soluble derivative of vitamin C and vitamin E, attenuated oxidative injury and prevents cells from apoptosis. The results suggest that EPC-K1 might be used as a potential therapeutic agent for diseases associated with NO/ONOO(-)-mediated neuronal injury.
过氧亚硝酸盐诱导培养的小脑颗粒细胞凋亡，在形态学上通过染色质凝聚得以证实，在生物化学上通过DNA梯状条带得以证实。暴露于过氧亚硝酸盐（10微摩尔）30分钟引发氧化应激，导致硫代巴比妥酸反应性物质（TBARS）的形成以及细胞膜流动性的改变。过氧亚硝酸盐处理还导致ATP减少，从而激活凋亡程序。用抗氧化剂EPC-K1（L-抗坏血酸2-[3,4-二氢-2,5,7,8-四甲基-2-(4,8,12-三甲基十三烷基)-2H-1-苯并吡喃-6-基-氢磷酸]钾盐）预处理细胞，EPC-K1是维生素C和维生素E的一种新的水溶性衍生物，可减轻氧化损伤并防止细胞凋亡。结果表明，EPC-K1可能用作与NO/ONOO(-)介导的神经元损伤相关疾病的潜在治疗剂。
