Bravo C, Chávez E, Rodríguez J S, Moreno-Sánchez R
Departamento de Bioquímica, Instituto Nacional de Cardiología, México D.F., Mexico.
Comp Biochem Physiol B Biochem Mol Biol. 1997 May;117(1):93-9. doi: 10.1016/s0305-0491(96)00257-x.
The membrane permeability transition (MPT) induced by Ca2+ and Pi or Asi was studied in rat kidney mitochondria. Membrane potential, Ca2+ transport and swelling were used to monitor the MPT. Asi promoted a faster and more extensive collapse of membrane potential, Ca2+ release and swelling than Pi. The MPT induced by Pi was fully blocked by Mg(2+)+ADP, spermine+ADP, Mg(2+)+ cyclosporin A (CSA), and ADP+CSA. In contrast, the MPT induced by Asi was only prevented, although not completely, by CSA+Mg2+ or ADP+CSA. Asi, but not Pi, was able to cause collapse of membrane potential in the presence of Sr2+. Carboxyatractyloside (CAT) produced collapse of membrane potential at a lower concentration in the presence of Asi+Ca(2+)+ADP than with Pi+Ca(2+)+ADP. The addition of Pi+Ca2+ to [14C]-ADP loaded mitochondria brought about a greater ADP release than Asi+Ca2+. The ADP release was CAT-sensitive with Pi but it was only partially blocked by Asi. The diminution of external pH did not inhibit the MPT induced by Pi or Asi. The results of this study suggest that the adenine nucleotide translocase does not have an essential role in the MPT induced by Asi+Ca2+.
在大鼠肾线粒体中研究了由Ca2+、Pi或Asi诱导的膜通透性转变(MPT)。利用膜电位、Ca2+转运和肿胀来监测MPT。与Pi相比,Asi能促进膜电位更快、更广泛地崩溃、Ca2+释放和肿胀。Pi诱导的MPT被Mg(2+)+ADP、精胺+ADP、Mg(2+)+环孢素A(CSA)和ADP+CSA完全阻断。相比之下,Asi诱导的MPT仅被CSA+Mg2+或ADP+CSA部分阻止,而非完全阻止。在存在Sr2+的情况下,Asi而非Pi能够导致膜电位崩溃。在Asi+Ca(2+)+ADP存在时,羧基苍术苷(CAT)在较低浓度下就能引起膜电位崩溃,而在Pi+Ca(2+)+ADP存在时则不然。向加载了[14C]-ADP的线粒体中添加Pi+Ca2+比添加Asi+Ca2+能导致更多的ADP释放。Pi引起的ADP释放对CAT敏感,但Asi仅能部分阻断该释放。外部pH的降低并不抑制Pi或Asi诱导的MPT。本研究结果表明,腺嘌呤核苷酸转位酶在Asi+Ca2+诱导的MPT中不起关键作用。