THE BIOCHEMICAL BASIS OF THE CLINICAL INTERACTION OF Fe DEFICIENCY AND Pb INTOXICATION

In children, iron (Fe) deficiency and lead (Pb) intoxication often coexist and aggravate each other; the elevation of erythrocyte porphyrin induced by Pb is much made prominent by Fe deficiency. We studied the interaction of Pb and Fe on ferrochelatase, the mitochondrial enzyme that catalyzes the incorporation of Fe into protoporphyrin. Mitochondria were isolated from reticulocytes of patients with sickle-cell syndromes undergoing therapeutic exchange transfusions. Enzyme kinetics of ferrocpelatase were then studied on freeze-thawed preparations by measuring the incorporation of 59Fe into heme. In the absence of Pb. the KmFe was 13 μM. and Vmax was .021 μM/min/mg protein. In the presence of varying concentrations of Pb. the Ki was estimated at 50 μM. As concentrations of Pb were progressively decreased from 100 μM to 1 μM, in the presence of various Fe concentrations, the effect of Pb became much more pronounced as the Fe concentration decreased. At Pb concentrations between 10 μM and 1 μM (corresponding to 200 20 μg/dl) a more marked inhibition could be demonstrated when the Fe concentration was below 10 μM.