Cardiotoxicity of parenterally administered iron complexes.

The role of cell calcium overload in the cardiotoxicity of low molecular weight iron complexes has been studied using 45Ca(2+)-uptake determinations in mice intraperitoneally injected with ferric lactate and ferric-ATP complex. Heart tissue shows a very high increase of 45Ca(2+)-uptake which appears to corroborate the hypothesis of cardiotoxicity by calcium overload. ATP seems to play a role in the degree of iron complex efficiency as cell calcium homeostasis modifier.