Regulation of free Ca2+ by subcellular fractions of rat incisor odontoblasts.
A miniaturized Ca2+ electrode system was developed to monitor small and fast fluctuations of Ca2+ activity in the micromolar range in 100 microliters volumes. This was used to study Ca2+ influx/efflux cycling in suspensions of rat-odontoblast and liver-cell mitochondria and microsomes, as well as in whole odontoblasts with plasma membranes made permeable by digitonin. The steady-state free-Ca2+ activity maintained by mitochondria was pCa 6.2-6.4, and that of microsomes pCa 6.4-6.6. These levels were held upon repeated additions of Ca2+ and EGTA. The odontoblast mitochondria and microsomes had an intracellular Ca2+ buffering capacity similar to that of liver cells. The steady-state pCa level maintained in suspensions of digitonin-permeabilized whole odontoblasts was 6.4-6.6. Thus, this study gave no evidence for any specialized intracellular handling of Ca2+ in cells involved in mineralization.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007180:Incisor / Q000378:metabolism; D008861:Microsomes / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D009804:Odontoblasts / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013347:Subcellular Fractions / Q000378:metabolism
D002118:Calcium