Machida Kiyotaka, Osada Hiroyuki
Antibiotics Laboratory, Riken, Hirosawa 2-1, Saitama 351-0198, Japan.
Ann N Y Acad Sci. 2003 Dec;1010:182-5. doi: 10.1196/annals.1299.031.
We propose a model for the mechanism of permeability transition (PT) related cytochrome c release. It is likely that the Ca(2+) requirement for the induction of the mitochondrial permeability transition pore (MPTP) opening might be due to the Ca(2+)-dependent interaction between cyclophilin D and ANT. We show here that the modification of adenine nucleotide translocase (ANT), which is one of the components of MPTP, can induce two different types of the cytochrome c release. One is dependent on classical PT, resulting in mitochondrial swelling, and is inhibited by cyclosporin A. The other is PT-independent, without swelling, and is insensitive to cyclosporin A.
我们提出了一种与通透性转换（PT）相关的细胞色素c释放机制的模型。诱导线粒体通透性转换孔（MPTP）开放对Ca(2+)的需求，可能是由于亲环蛋白D与腺嘌呤核苷酸转位酶（ANT）之间的Ca(2+)依赖性相互作用。我们在此表明，MPTP的组成成分之一——腺嘌呤核苷酸转位酶（ANT）的修饰，可诱导两种不同类型的细胞色素c释放。一种依赖于经典的PT，导致线粒体肿胀，并被环孢素A抑制。另一种不依赖于PT，无肿胀现象，且对环孢素A不敏感。
