Fulceri R, Gamberucci A, Bellomo G, Giunti R, Benedetti A
Instituto di Patologia Generale, University of Siena, Italy.
Biochem J. 1993 Nov 1;295 ( Pt 3)(Pt 3):663-9. doi: 10.1042/bj2950663.
The effect of CoA and fatty acyl-CoA esters on Ca2+ fluxes has been studied in isolated liver microsomes and in digitonin-permeabilized hepatocytes. When microsomes were loaded with increasing concentrations of Ca2+ (6-29 nmol/mg of protein), the extent to which CoA and palmitoyl-CoA released Ca2+ increased. At 23 nmol of Ca2+/mg of protein, half-maximal [CoA] and [palmitoyl-CoA] were 35 and 50 microM respectively. Under conditions of minimal Ca2+ loading, net release of Ca2+ was absent, but Ca2+ translocation from a CoA-sensitive to a CoA-insensitive pool took place. The effect of CoA required the presence of fatty acids, probably to form fatty acyl esters. In permeabilized hepatocytes, the pool(s) mobilized by CoA (or by palmitoyl-CoA) appeared to be different from that mobilized by Ins(1,4,5)P3.
已在分离的肝微粒体和洋地黄皂苷通透的肝细胞中研究了辅酶A（CoA）和脂肪酰辅酶A酯对钙离子通量的影响。当向微粒体中加载浓度不断增加的钙离子（6 - 29纳摩尔/毫克蛋白质）时，CoA和棕榈酰辅酶A释放钙离子的程度增加。在23纳摩尔钙离子/毫克蛋白质时，CoA和棕榈酰辅酶A的半数最大浓度分别为35和50微摩尔。在钙离子负载量最小的条件下，不存在钙离子的净释放，但钙离子从对CoA敏感的池转移到了对CoA不敏感的池。CoA的作用需要脂肪酸的存在，可能是为了形成脂肪酰酯。在通透的肝细胞中，由CoA（或棕榈酰辅酶A）动员的池似乎与由肌醇-1,4,5-三磷酸（Ins(1,4,5)P3）动员的池不同。
