The distribution of Ca2+ in intact cells was monitored with fluorescent probes: fura-2 for cytosolic [Ca2+] and rhod-2 for mitochondrial [Ca2+]. It was found that in neoplastic cells, such as Ehrlich ascites tumour and Zajdela hepatoma, but not in non-malignant cells, such as fibroblasts, glucose and deoxyglucose elicited release of Ca2+ from endoplasmic reticulum stores and an increase in Ca2+ concentration in the cytosol. Parallel to this, a decrease in the rate of Ca2+ extrusion from the cell and an enhanced uptake of Ca2+ by mitochondria were observed. The increase in mitochondrial [Ca2+] was accompanied by an increase in the mitochondrial membrane potential and the reduction state of nicotinamide nucleotides. F1F0-ATPase in submitochondrial particles of Zajdela hepatoma was strongly inhibited in the presence of micromolar Ca2+ concentrations, whereas this activity in submitochondrial particles from rat liver appeared to be less sensitive to Ca2+. Indications of glycosylation of Ehrlich ascites tumour cell proteins were also obtained. These data strengthen the proposal [Bogucka, K., Teplova, V.V., Wojtczak, L. and Evtodienko, Y. V. (1995) Biochim. Biophys. Acta 1228, 261-266] that the Crabtree effect is produced by mobilization of cell calcium, which is subsequently taken up by mitochondria and inhibits F1F0-ATP synthase.
