Kondoh M, Aoki Y, Ogawa Z, Hata Y, Suzuki H, Itoh H
Kitasato Arch Exp Med. 1989 Dec;62(4):181-6.
Cholestatic liver injury was experimentally induced in rats by administration of chlorpromazine (CPZ). The peak activity of mitochondrial aspartate aminotransferase (AST) released in serum was found to precede the peak of total AST activity. The liver mitochondria obtained from rats treated with CPZ was fractionated into two subfractions: one containing the intermembrane space, and the other containing the matrix and the membranes. As a results, the relative activity of AST in the intermembrane space was significantly increased at 12 h after CPZ administration. This result suggests that mitochondrial AST, which is dominantly located in the mitochondrial matrix, transmigrated to the intermembrane space via the inner membrane under the effect of CPZ administration.
通过给予大鼠氯丙嗪(CPZ)实验性诱导胆汁淤积性肝损伤。发现血清中释放的线粒体天冬氨酸氨基转移酶(AST)的峰值活性先于总AST活性的峰值出现。从用CPZ处理的大鼠获得的肝线粒体被分离成两个亚组分:一个包含膜间隙,另一个包含基质和膜。结果,在给予CPZ后12小时,膜间隙中AST的相对活性显著增加。该结果表明,主要位于线粒体基质中的线粒体AST在CPZ给药的作用下通过内膜迁移到膜间隙。