Lepore D A, Stewart A G, Tomasi A, Anderson R L, Hurley J V, Morrison W A
Bernard O'Brien Institute of Microsurgery, St. Vincent's Hospital, Fitzroy, Melbourne, 3065, Australia.
Nitric Oxide. 1999 Aug;3(4):273-80. doi: 10.1006/niox.1999.0239.
The survival of skeletal muscle myoblasts in culture after exposure either to a donor of NO, sodium nitroprusside (SNP), or ethanamine, 2,2'-(hydroxynitrosohydrazono)bis-(DETA NONOate), or to a donor of both NO and O(-)(2), 3-morpholinosydnonimine hydrochloride (SIN-1), was investigated. SIN-1 reduced clonogenic survival markedly but donors of NO alone did not. The injurious effect of SIN-1 was prevented by oxyhemoglobin or by uric acid but not by superoxide dismutase. The exposure of myoblasts to authentic peroxynitrite (ONOO(-)) or to DETA NONOate in the presence of an O(-)(2)-generating system did not reduce their survival. The results show that NO or ONOO(-) alone is not detrimental to myoblast survival and suggest that SIN-1 toxicity is, at least in part, mediated by H(2)O(2) in this myoblast culture system.
研究了骨骼肌成肌细胞在培养中暴露于一氧化氮供体(硝普钠(SNP)或乙胺,2,2'-(羟基亚硝基肼基)双-(二乙三胺 NONO 酸盐))或一氧化氮和超氧阴离子(O⁻²)供体(盐酸 3-吗啉代 sydnonimine(SIN-1))后的存活情况。SIN-1 显著降低了克隆形成存活率,但单独的一氧化氮供体则没有。SIN-1 的损伤作用可被氧合血红蛋白或尿酸阻止,但不能被超氧化物歧化酶阻止。在存在 O⁻²生成系统的情况下,将成肌细胞暴露于纯过氧亚硝酸盐(ONOO⁻)或二乙三胺 NONO 酸盐不会降低它们的存活率。结果表明,单独的一氧化氮或过氧亚硝酸盐对成肌细胞存活无害,并表明在该成肌细胞培养系统中,SIN-1 的毒性至少部分由过氧化氢介导。