Saris N E, van den Bosch H
Department of Medical Chemistry, University of Helsinki, Finland.
J Bioenerg Biomembr. 1988 Dec;20(6):749-57. doi: 10.1007/BF00762551.
Respiring rat liver mitochondria are known to spontaneously release the Ca2+ taken up when they have accumulated Ca2+ over a certain threshold, while Sr2+ and Mn2+ are well tolerated and retained. We have studied the interaction of Sr2+ with Ca2+ release. When Sr2+ was added to respiring mitochondria simultaneously with or soon after the addition of Ca2+, the release was potently inhibited or reversed. On the other hand, when Sr2+ was added before Ca2+, the release was stimulated. Ca2+-induced mitochondrial damage and release of accumulated Ca2+ is generally believed to be due to activation of mitochondrial phospholipase A (EC 3.1.1.4.) by Ca2+. However, isolated mitochondrial phospholipase A activity was little if at all inhibited by Sr2+. The Ca2+-release may thus be triggered by some Ca2+-dependent function other than phospholipase.
已知呼吸状态的大鼠肝脏线粒体在积累的Ca2+超过一定阈值时会自发释放所摄取的Ca2+，而Sr2+和Mn2+则能被很好地耐受并保留。我们研究了Sr2+与Ca2+释放的相互作用。当在加入Ca2+的同时或之后不久将Sr2+加入到呼吸的线粒体中时，Ca2+的释放被强烈抑制或逆转。另一方面，当在加入Ca2+之前加入Sr2+时，Ca2+的释放则受到刺激。Ca2+诱导的线粒体损伤和积累的Ca2+释放通常被认为是由于Ca2+激活了线粒体磷脂酶A（EC 3.1.1.4.）。然而，Sr2+对分离的线粒体磷脂酶A活性几乎没有抑制作用。因此，Ca2+的释放可能是由磷脂酶以外的某种Ca2+依赖性功能触发的。
