bis(1-3-dibutylbarbiturate)trimethine-oxonol and indo-1

CD3 mAb induced calcium movements are unaffected by hyperpolarization of the membrane in Jurkat T cells treated with valinomycin. By contrast, the CD3 induced Ca2+ influx was impaired by depolarization of the membrane with either gramicidin or by equimolar substitution of KCl for NaCl in the medium. In depolarized cells, the synthesis of phosphatidylserine was strongly diminished as a result of impaired transport of the [3H]serine substrate. In depolarized cells, the CD3-induced release of Ca2+ from intracellular stores (endoplasmic reticulum) was unaffected. Emptying of the Ca2+ stores by CD3 was shown by the lack of effect of additional treatment of the cells with the Ca2+ ionophore, ionomycin. The empty status of the calcium stores was also confirmed by measurements of phosphatyidylserine synthesis through the Ca2+ -dependent base exchange enzyme system that was found to be significantly decreased despite the low amount synthesized in the presence of a defective [3H]serine transport in depolarized cells.

Topics: Antibodies, Monoclonal; Barbiturates; Calcium; CD3 Complex; Fluorescent Dyes; Gramicidin; Humans; Indoles; Ionomycin; Ionophores; Isoxazoles; Jurkat Cells; Membrane Potentials; Phosphatidylserines; T-Lymphocytes; Valinomycin