MECHANISMS OF THE TOXIC EFFECT OF LEAD .1. FREE LEAD IN ERYTHROCYTE

In this work, a selection of children was examined based on their free erythrocyte protoporphyrin (FEP) and total blood lead (PbB) contents. Two groups with clear differences in lead sensibility were selected. One group with high FEP levels (deep lead alteration), named ''normal,'' and one group with low FEP levels (discrete lead alteration), named ''lead tolerant, '' and both with similar PbB concentration, were formed. The selection, based on FEP level, showed a correlation with other indicators (neuromotor alterations). A lower activity of the enzymes Glyceraldehyde 3-phosphate dehydrogenase (GA3PD), Glucose 6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), and Lactate dehydrogenase (LDH) was found in the normal group when compared to the tolerant group. Therefore, the influence of the lead acetate upon the same erythrocyte enzyme activities was investigated. Lead inhibition of the enzymes GA3PD and G6PD was found, and this inhibition could be related to the free lead content found in the erythrocytes. Inhibition of the enzymes 6PGD and LDH was also found, but these enzymes were not inhibited by exposure to lead acetate. Erythrocyte free lead content was high in the normal group when compared to the lead tolerant group and could be a determinant factor in the biochemical alterations found. Low erythrocyte free lead contents could be an indicator of lead tolerance. TCA-precipitation was found to be a useful method to evaluate free lead content; it gave similar results to gel filtration molecular chromathography.