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PubMed1998

Plasma and blood lead in humans: capacity-limited binding to delta-aminolevulinic acid dehydratase and other lead-binding components.

In 42 lead-exposed workers (22 male and 20 female), we found a close nonlinear relation between blood and plasma lead concentrations, determined by inductively coupled plasma mass spectrometry (ICP-MS). The concentration medians and ranges were lead in whole blood, 270 (97 to 950) micrograms/L and lead in plasma, 1.1 (0.2 to 13) micrograms/L. Proteins from lysed erythrocytes were studied by gel chromatography with ICP-MS detection. We then found capacity-limited binding for lead to delta-aminolevulinic acid dehydratase (ALAD), as well as to two other components (with apparent molecular masses of 45 and < 10 kDa, respectively). The strongest affinity for lead was indicated for ALAD (35-81% of the lead in blood) and could be described by a capacity of 850 micrograms/L and a dissociation constant of 1.5 micrograms/L. The 45-kDa protein carried 12-26% of the blood lead, and the < 10-kDa component less than 1%. A model based on these three components, plus a fourth one for unrecovered lead (2-45%), is proposed. No binding of lead to hemoglobin was found. There was an association between zinc and lead in whole blood; however, zinc did not significantly affect the lead distribution in erythrocytes.

Chromatography, Gel↗
PubMed1980

Lead in blood and tissues of mice after administration of low lead doses.

Lead levels in whole blood could be determined reliably up to a lower limit of 2 micrograms/100 ml blood, using a modified micromethod of the graphite tube furnace technique. Lead contents of various tissues were also determined by using the automated graphite tube furnace after wet ashing of the organs with nitric acid in autoclaves. Animal experiments with mice showed no measurable increase in blood lead level after a single, 10- or 30-days oral administration of lead in doses of 10--1000 micrograms lead acetate/kg body weight/day. However, these doses led to a rise in tissue lead content. There was a clear dependence of tissue lead content on type of organ examined, lead dose and duration of lead exposure. According to our experiments, the threshold dose which leads to a long-term increase in tissue lead content is assumed to be about 100 micrograms lead acetate/kg body weight/day, orally administered.

Animals↗