Shidoji Y, Hayashi K, Komura S, Ohishi N, Yagi K
Gifu International Institute of Biotechnology, Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, Gifu, 505-0116, Japan.
Biochem Biophys Res Commun. 1999 Oct 22;264(2):343-7. doi: 10.1006/bbrc.1999.1410.
To explore the molecular mechanism underlying the translocation of cytochrome c from the mitochondrial inner membrane to the cytosol during apoptosis, we analyzed the molecular interaction between cytochrome c and cardiolipin (CL) by (1)H NMR spectroscopy. Bovine heart CL induced a drastic broadening of the linewidth of the downfield signals at 31.4 and 34.2 ppm assigned to the heme methyl group-3 and -8, respectively, of horse heart cytochrome c. In contrast, CL mono- and dihydroperoxides were less active in broadening the signals than CL, and CL trihydroperoxides induced almost no broadening of their linewidth. This finding suggests that the peroxidation of CL induces a release of cytochrome c from mitochondria into the cytosol, which release induces apoptosis in the cells.
为了探究细胞凋亡过程中细胞色素c从线粒体内膜转移至胞质溶胶的分子机制，我们通过核磁共振氢谱（¹H NMR）分析了细胞色素c与心磷脂（CL）之间的分子相互作用。牛心CL使马心细胞色素c中分别归属于血红素甲基-3和-8的位于31.4和34.2 ppm处的低场信号的线宽急剧变宽。相比之下，CL单氢过氧化物和二氢过氧化物在使信号变宽方面的活性低于CL，而CL三氢过氧化物几乎未使其线宽变宽。这一发现表明，CL的过氧化作用诱导细胞色素c从线粒体释放至胞质溶胶，这种释放诱导细胞凋亡。
