Schweizer M, Durrer P, Richter C
Laboratory of Biochemistry I, Swiss Federal Institute of Technology (ETH), Zürich.
Biochem Pharmacol. 1994 Aug 30;48(5):967-73. doi: 10.1016/0006-2952(94)90367-0.
Rat liver mitochondria contain a specific Ca2+ release pathway which operates when oxidized mitochondrial pyridine nucleotides are hydrolysed to ADPribose and nicotinamide. Here we report that the hydrophobic bifunctional thiol reagent phenylarsine oxide (PhAsO) at low concentrations stimulates this pathway by promoting a Ca(2+)-dependent hydrolysis of oxidized mitochondrial pyridine nucleotides. Ca2+ release is inhibited by cyclosporine A or m-iodobenzylguanidine, compounds known to prevent intramitochondrial pyridine nucleotide hydrolysis or protein mono(ADPribosyl)ation, respectively. At higher concentrations, PhAsO causes non-specific leakiness of mitochondria.
大鼠肝脏线粒体含有一种特定的Ca2+释放途径，当氧化型线粒体吡啶核苷酸水解为ADP核糖和烟酰胺时该途径发挥作用。在此我们报告，低浓度的疏水双功能硫醇试剂苯胂氧化物（PhAsO）通过促进氧化型线粒体吡啶核苷酸的Ca(2+)依赖性水解来刺激该途径。Ca2+释放受到环孢菌素A或间碘苄胍的抑制，已知这两种化合物分别可防止线粒体内吡啶核苷酸水解或蛋白质单（ADP核糖基）化。在较高浓度时，PhAsO会导致线粒体出现非特异性渗漏。
