Martinucci S, Szabò I, Tombola F, Zoratti M
Centro CNR Biomembrane e Dipartimento di Scienze Biomediche, Università di Padova, Padua, Italy.
FEBS Lett. 2000 Sep 1;480(2-3):89-94. doi: 10.1016/s0014-5793(00)01911-6.
Ubiquinone 0 and decylubiquinone have been reported to inhibit the mitochondrial permeability transition pore (PTP) [Fontaine, E., Ichas, F. and Bernardi, P. (1998) J. Biol. Chem. 273, 25734-257401, offering a new clue to its molecular composition. In patch-clamp experiments on rat liver mitochondria we have observed that these compounds also inhibit the previously described mitochondrial megachannel (MMC), confirming its identification as the PTP. Inhibition can be reversed by increasing [Ca2+], in analogy to the behavior observed with several other disparate PTP/MMC inhibitors. To rationalize the ability of Ca2+ to overcome inhibition by various quite different compounds we propose that it acts via the phospholipid bilayer.
据报道，泛醌0和癸基泛醌可抑制线粒体通透性转换孔（PTP）[方丹，E.，伊查斯，F.和贝尔纳迪，P.（1998年）《生物化学杂志》273，25734 - 257401]，为其分子组成提供了新线索。在对大鼠肝线粒体进行的膜片钳实验中，我们观察到这些化合物还抑制了先前描述的线粒体大通道（MMC），证实其可被鉴定为PTP。与其他几种不同的PTP/MMC抑制剂所观察到的行为类似，增加[Ca2+]可逆转抑制作用。为了合理解释Ca2+克服各种截然不同化合物抑制作用的能力，我们提出它是通过磷脂双层起作用的。
