Harris E J
Biochem J. 1977 Dec 15;168(3):447-56. doi: 10.1042/bj1680447.
The kinetics of uptake of Ca(2+) by rat heart mitochondria were studied by a spectrophotometric method with Arsenazo III indicator. The exponential rate coefficients measured with or without added phosphate increase with the amount of Ca(2+) added up to about 24mum. Evidence is given that the effect is attributable to a combination of formation of chelates at low concentrations to act as Ca(2+) buffers, with co-transport of substrate to provide more respiratory fuel. The inhibitory effect of Mg(2+) depends on the Ca(2+) concentration, so with a constant [Mg(2+)] the low concentrations of Ca(2+) are most inhibited, and the rate coefficients are still more Ca(2+)-dependent. Ca(2+) uptake is slowed by local anaesthetics such as butacaine and dibucaine, and also by propranolol and palmitoyl-CoA. After an uptake, the release of Ca(2+) was investigated. The spontaneous release involves an initially slow and small appearance of free Ca(2+) and is followed by an auto-accelerated phase. The release is accompanied by a gradual decrease in internal ATP; it is initiated by palmitoyl-CoA (reversed by carnitine), by lysophosphatidylcholine, by Na(+) salts (reversed by oligomycin) and by K(+) salts added to a K(+)-free medium containing valinomycin. The process is probably a response to an increased energy load imposed on the mitochondria by the various conditions, which include the spontaneous action of phospholipase activated by traces of Ca(2+). The problem of how much mitochondrial activity is participating in normal heart Ca(2+) turnover is discussed, and experiments showing only 7-14% exchange of the mitochondrial Ca(2+) occurring in vivo in 10 or 20min are reported.
采用偶氮胂III指示剂分光光度法研究了大鼠心脏线粒体对Ca(2+)的摄取动力学。添加或不添加磷酸盐时测得的指数速率系数随添加的Ca(2+)量增加，直至约24μm。有证据表明，这种效应归因于低浓度时螯合物形成以充当Ca(2+)缓冲剂与底物协同转运以提供更多呼吸燃料的综合作用。Mg(2+)的抑制作用取决于Ca(2+)浓度，因此在[Mg(2+)]恒定的情况下，低浓度的Ca(2+)受抑制最明显，且速率系数对Ca(2+)的依赖性更强。丁卡因和地布卡因等局部麻醉剂以及普萘洛尔和棕榈酰辅酶A会减缓Ca(2+)的摄取。摄取后，对Ca(2+)的释放进行了研究。自发释放最初涉及游离Ca(2+)缓慢少量出现，随后是自动加速阶段。释放伴随着内部ATP逐渐减少；它由棕榈酰辅酶A（肉碱可逆转）、溶血磷脂酰胆碱、钠盐（寡霉素可逆转）以及添加到含缬氨霉素的无钾培养基中的钾盐引发。该过程可能是对各种条件施加于线粒体的能量负荷增加的一种反应，这些条件包括痕量Ca(2+)激活的磷脂酶的自发作用。讨论了正常心脏Ca(2+)周转中线粒体活性参与程度的问题，并报告了在10或20分钟内体内仅发生7 - 14%线粒体Ca(2+)交换的实验。
