ON THE MECHANISM OF SOFT-TISSUE CALCIFICATION INDUCED BY COMPLEXED IRON

The interaction of ferric lactate with Ehrlich carcinoma ascites cells induces a modification of Ca2+-uptake which is in direct relationship with the iron mass bound to die cells. Competitive binding of iron by deferoxamine indicates that only a part of the bound iron penetrates the cell, and that to trigger a Ca2+-influx this intracellular iron mu st be over a threshold concentration. The experimental finding that fe rric lactate transfers its iron to albumin and to ATP suggests that in the Ca2+-uptake modification it works through its iron transfer which provokes the inhibition of the cell calcium homeostasis regulatory sy stems (Ca2+-channels, intracellular Ca2+-binding sites and Ca2+-pump A TPase). The involvement of ATP in the action of ferric lactate seems r elated to a higher stability of the complex, and to a larger availabil ity of active iron able to perform the inhibitory process.