Richter C, Schlegel J, Schweizer M
Laboratory of Biochemistry I, Swiss Federal Institute of Technology (ETH), Zürich.
Ann N Y Acad Sci. 1992 Nov 21;663:262-8. doi: 10.1111/j.1749-6632.1992.tb38669.x.
Ca2+ release from mitochondria can be induced by a variety of chemically different prooxidants. Release induced by these compounds is possibly regulated by protein mono(ADP)ribosylation, and leaves mitochondria initially intact. Excessive "cycling" (continuous release and uptake) of Ca2+ by mitochondria leads to their damage, as shown by a decreased membrane potential, fast Ca2+ release, and impairment of ATP synthesis. When cycling is prevented by Ca2+ chelators or by inhibition of the uptake route with ruthenium red, prooxidants still induce Ca2+ release but mitochondria remain intact. It has recently been suggested that formation of a "pore" in the inner mitochondrial membrane participates in the Ca2+ release mechanism. We find that the prooxidant-induced Ca2+ release is not paralleled by sucrose entry into, or K+ release from, or swelling of mitochondria, provided Ca2+ cycling is prevented. Thus, the prooxidant-induced Ca2+ release does not require formation of a "pore." We conclude that the release occurs via a specific pathway.
多种化学性质不同的促氧化剂均可诱导线粒体释放Ca2+。这些化合物诱导的释放可能受蛋白质单（ADP）核糖基化调节，且最初线粒体保持完整。线粒体对Ca2+的过度“循环”（持续释放和摄取）会导致其受损，表现为膜电位降低、Ca2+快速释放以及ATP合成受损。当通过Ca2+螯合剂或用钌红抑制摄取途径来阻止循环时，促氧化剂仍可诱导Ca2+释放，但线粒体保持完整。最近有人提出线粒体内膜上形成“孔道”参与了Ca2+释放机制。我们发现，只要阻止Ca2+循环，促氧化剂诱导的Ca2+释放就不会伴随蔗糖进入线粒体、K+从线粒体释放或线粒体肿胀。因此，促氧化剂诱导的Ca2+释放不需要形成“孔道”。我们得出结论，释放是通过特定途径发生的。
