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 Ca(2+)-uptake which is in direct relationship with the iron mass bound to the cells. Competitive binding of iron by deferoxamine indicates that only a part of the bound iron penetrates the cell, and that to trigger a Ca(2+)-influx this intracellular iron must be over a threshold concentration. The experimental finding that ferric lactate transfers its iron to albumin and to ATP suggests that in the Ca(2+)-uptake modification it works through its iron transfer which provokes the inhibition of the cell calcium homeostasis regulatory systems (Ca(2+)-channels, intracellular Ca(2+)-binding sites and Ca(2+)-pump ATPase). The involvement of ATP in the action of ferric lactate seems related to a higher stability of the complex, and to a larger availability of active iron able to perform the inhibitory process.