Abstract

Lead has been reported to poison many enzyme systems including the Na+K dependent ATPase essential to maintaining normal membrane potentials. The present study was designed to measure the toxic effects of lead on membrane trnaspor in human erythrocytes resulting from possible changes in ATPase activity. Na flux and membrane Na+K dependent. ATPase were measured in erythrocytes of patients with lead poisoning and in normal erythrocytes exposed in vitro to lead in concentrations of 50–200 micrograms/100 ml. We have not been able to confirm the presence of decreased. ATPase activity in patients with mild lead poisoning (i.e. no encephalopathy and blood concentrations of lead between 60 and 90 micrograms/100 ml.). However, we have demonstrated a markedly increased passive Na leak in both erythrocyte ghosts and intact cells. Active outward Na transport was also increased perhaps as a compensatory mechanism. In vitro exposure of intact red cells to lead has produced similar increases in membrane permeability to Na. In addition, when lead is incorporated in vitro into erythrocyte ghosts inhibition of active transport can be demonstrated. The mechanisms producing the two different effects of lead on membrane transport are separable and may be dose dependent. Thus lead affects the membrane in addition to any possible enzyme injury.

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