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