Chernyak B V, Dedov V N
A. N. Belozersky Institute of Physico-Chemical Biology, Moscow State University, Russian Federation.
FEBS Lett. 1995 May 22;365(1):75-8. doi: 10.1016/0014-5793(95)00411-2.
The opening of the cyclosporin A-sensitive permeability transition pore (MTP) in deenergized mitochondria was induced only at millimolar Ca2+. Pretreatment of the mitochondria with 'inducers', such as duroquinone and phenylarsine oxide, allowed observing the pore opening at 0.01-0.1 mM Ca2+. Duroquinone caused a rapid (within 20 s) NAD(P)H oxidation which was followed by a slow (20 min) induction of the pore sensitive to low Ca2+. Phenylarsine oxide capable of cross-linking of vicinal SH-groups caused pore formation without the oxidation of NAD(P)H. The pore opening by both 'inducers' was prevented by N-ethylmaleimide. We propose that oxidation or cross-linking of critical dithiol(s) in membrane proteins increase the sensitivity of a putative 'Ca(2+)-sensor' that regulates the permeability transition pore opening.
仅在毫摩尔浓度的钙离子条件下，去能化线粒体中环孢菌素A敏感的通透性转换孔（MTP）才会开放。用“诱导剂”（如杜醌和苯胂酸氧化物）预处理线粒体后，可在0.01 - 0.1 mM钙离子浓度下观察到孔的开放。杜醌导致快速（20秒内）的NAD(P)H氧化，随后是缓慢（20分钟）诱导对低钙离子敏感的孔。能够交联相邻巯基的苯胂酸氧化物可导致孔的形成，而不会使NAD(P)H氧化。两种“诱导剂”引起的孔开放均被N - 乙基马来酰亚胺阻止。我们提出，膜蛋白中关键二硫醇的氧化或交联会增加假定调节通透性转换孔开放的“钙离子传感器”的敏感性。
