自由基对红细胞钙调机制的影响  

EFFECT OF FREE RADICAL ON CALCIUM REGULATION IN RED BLOOD CELLS

作　　者：黄益民[1] 刘丹晶[1] 刘舒[1] 孙芳臻[2] 辛俭[2] 

机构地区：[1]北京市心肺血管疾病研究所,北京100029 [2]中国科学院发育研究所,北京100080

出　　处：《生物物理学报》1999年第3期573-578,共6页Acta Biophysica Sinica

基　　金：国家自然科学基金;北京市自然科学基金

摘　　要：为探讨自由基对红细胞钙调机制的影响， 采用荧光标记的方法， 分别观察了健康人的红细胞在单纯Ｆｅｎｔｏｎ 反应体系作用下和钙通道阻断剂＋ Ｆｅｎｔｏｎ 体系作用下胞内钙浓度的动态变化。发现：（１） 在Ｆｅｎｔｏｎ 体系开始作用２ ～３ 分钟后，红细胞内钙浓度才突然地急剧增加，此后便维持在一个明显低于胞外浓度的稳定水平；（２） 在Ｆｅｎｔｏｎ 体系作用前后， 采用钙通道阻断剂镍可防止胞内钙的增加或使胞内钙浓度逐渐降至作用前水平。以上结果说明， 在Ｆｅｎｔｏｎ 体系作用下， 红细胞仍保持对胞内异常高钙的清除能力。In order to investigate the effect of free radical on calcium (Ca2+) regulation in red blood cells (RBCs), we used a fluorescent probe-Fura2, to evaluate dynamically changes of RBC's Ca2+ when either reacted with Fenton system or interfered by calcium channel bloker-Ni2+. Result showed that (1) after reacted with Fenton system for two to three minutes, a fasting increase of intracellular Ca2+ appeared and then kept at stable a level around 300 nmol but still was significantly lower than the extracellular. (2) Pre- or Post-reacted with Fenton system, Ni2+ either inhibited intracellular Ca2+ enhancement or gradually reduced high intracellular Ca2+ introduced by Fenton system to normal. The study shows that under the action of Fenton system damaging, RBC is still capable of discharging intracellular abnormal Ca2+, demonstrating that free radical did not result in complete damage of RBC Ca2+ regulation in dysfunction.

关 键 词：自由基 红细胞 钙调机制 

分 类 号：Q592.1[生物学—生物化学] Q505