Grist E M, Baum H
Eur J Biochem. 1975 Sep 15;57(2):621-6. doi: 10.1111/j.1432-1033.1975.tb02338.x.
The halothane-dependent, calcium-induced loss of respiratory control in rat liver mitochondria [1, 2] is Mg2plus -dependent and is accompanied by an enhanced mitochondrial swelling. It is suggested that this swelling reflects an increase in calcium activity in the matrix space, due to a decrease in binding of the accumulated cation. This change in the partition of intramitochondrial calcium is correlated with an inhibition by halothane of energy-independent, calcium-induced swelling. The enhanced swelling associated with the active accumulation of calcium in the presence of halothane does not lead to a marked increase in permeability to other ions. Nevertheless, under conditions of energised calcium uptake, and in the presence of Mg2plus, a halothane-dependent, ruthenium red-insensitive efflux of calcium is observed. This is consistent with the proposed halothane-dependent increase in the matrix activity of accumulated Ca2plus. It is suggested that this mechanism accounts for the previously postulated [2] futile cycle of calcium uptake and release induced by halothane in rat liver mitochondria.
大鼠肝线粒体中氟烷依赖性、钙诱导的呼吸控制丧失[1,2]是镁离子依赖性的，且伴有线粒体肿胀加剧。据推测，这种肿胀反映了基质空间中钙活性的增加，这是由于积累的阳离子结合减少所致。线粒体内钙分配的这种变化与氟烷对能量非依赖性、钙诱导的肿胀的抑制作用相关。在氟烷存在下，与钙的主动积累相关的肿胀加剧不会导致对其他离子的通透性显著增加。然而，在有能量的钙摄取条件下，且存在镁离子时，观察到氟烷依赖性、钌红不敏感的钙外流。这与所提出的氟烷依赖性积累的钙离子在基质中的活性增加是一致的。有人认为，这一机制解释了先前推测的[2]氟烷在大鼠肝线粒体中诱导的钙摄取和释放的无效循环。
