Department of Biochemistry, Kasturba Medical College, Manipal University, Manipal 576 104, India.
J Biosci. 2010 Dec;35(4):519-24. doi: 10.1007/s12038-010-0059-6.
Frog aortic tissue exhibits plasma membrane electron transport (PMET) owing to its ability to reduce ferricyanide even in the presence of mitochondrial poisons, such as cyanide and azide. Exposure to hypotonic solution (108 mOsmol/kg H2O) enhanced the reduction of ferricyanide in excised aortic tissue of frog. Increment in ferricyanide reductase activity was also brought about by the presence of homocysteine (100 microM dissolved in isotonic frog Ringer solution), a redox active compound and a potent modulator of PMET. Two plasma-membrane-bound channels, the volume-regulated anion channel (VRAC) and the voltage-dependent anion channel (VDAC), are involved in the response to hypotonic stress. The presence of VRAC and VDAC antagonists-tamoxifen, glibenclamide, fluoxetine and verapamil, and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS), respectively-inhibited this enhanced activity brought about by either hypotonic stress or homocysteine. The blockers do not affect the ferricyanide reductase activity under isotonic conditions. Taken together, these findings indicate a functional interaction of the three plasma membrane proteins, namely, ferricyanide reductase (PMET), VDAC and VRAC.
青蛙主动脉组织表现出质膜电子传递（PMET），因为它即使在存在线粒体毒物（如氰化物和叠氮化物）的情况下也能够还原铁氰化物。暴露于低渗溶液（108mOsmol/kg H2O）增强了青蛙离体主动脉组织中铁氰化物的还原。同型半胱氨酸（溶解在等渗青蛙林格溶液中的 100μM）的存在也导致了铁氰化物还原酶活性的增加，同型半胱氨酸是一种氧化还原活性化合物，也是 PMET 的有效调节剂。两种质膜结合通道，即体积调节阴离子通道（VRAC）和电压依赖性阴离子通道（VDAC），参与了对低渗应激的反应。VRAC 和 VDAC 拮抗剂-他莫昔芬、格列本脲、氟西汀和维拉帕米以及 4,4'-二异硫氰酸基二苯乙烯-2,2'-二磺酸（DIDS）分别抑制了由低渗应激或同型半胱氨酸引起的这种增强活性。这些阻断剂不会影响等渗条件下的铁氰化物还原酶活性。综上所述，这些发现表明三种质膜蛋白（即铁氰化物还原酶（PMET）、VDAC 和 VRAC）之间存在功能相互作用。
