COA AND FATTY ACYL-COA DERIVATIVES MOBILIZE CALCIUM FROM A LIVER RETICULAR POOL

The effect of CoA and fatty acyl-CoA esters on Ca2+ fluxes has been st udied in isolated liver microsomes and in digitonin-permeabilized hepa tocytes. When microsomes were loaded with increasing concentrations of Ca2+ (6-29 nmol/mg of protein), the extent to which CoA and palmiyoyl -CoA released Ca2+ increased. At 23 nmol of Ca2+/mg of protein, half-m aximal [CoA] and [palmitoyl-CoA] were 35 and 50 muM respectively. Unde r 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, pr obably to form fatty acyl esters. In permeabilized hepatocytes, the po ol(s) mobilized by CoA (or by palmitoyl-CoA) appeared to be different from that mobilized by Ins(1,4,5)P3.