Lead in plasma

Distribution. Lead in blood partitions between plasma and red blood cells, with the larger fraction (90-99%) associated with red blood cells (Cake et al. 1996 DeSilva 1981 Everson and Patterson 1980 Manton and Cook 1984 Ong and Lee 1980a). Lead in plasma binds to albumin and y -globulins (Ong and Lee 1980a). The fraction that is not bound to protein exists largely as complexes with low molecular weight sulfhydryl compounds these may include cysteine, homocysteine, and cysteamine (Al-Modhefer et al. 1991). Approximately 75% was bound to protein when whole human blood was incubated with 50 ig/dL lead (as lead chloride) approximately 90% of the bound lead was associated with albumin (Ong and Lee 1980a). However, the fraction of lead in plasma bound to protein would be expected to vary with the plasma lead concentration. 

The low concentrations of lead in plasma, relative to red blood cells, has made it extremely difficult to accurately measure plasma lead concentrations in humans, particularly at low PbB concentrations (i.e., less than 20 pg/dL). However, more recent measurements have been achieved with inductively coupled mass spectrometry (ICP-MS), which has a higher analytical sensitivity than earlier atomic absorption spectrometry methods. Using this analytical technique, recent studies have shown that plasma lead concentrations may correlate more strongly with bone lead levels than do PbB concentrations (Cake et al. 1996 Hemandez-Avila et al. 1998). The above studies were conducted in adults, similar studies of children have not been reported. 

Lead is absorbed to the blood plasma, and then rapidly equilibrates between plasma and the extracellular fluid. More slowly (but within minutes), lead is transferred from the plasma to the blood cells. The turnover of lead in plasma is very rapid, the half-life after intravenous injection in humans being 1 min (Campbell et al. 1984). Within the blood, about 99% of the Pb content is in the red cells, and less than 1% is in the plasma (Ong et al. 1990). In red blood cells, most of the inorganic lead is bound to 6-aminolevulinic acid (ALA Bergdahl et al. 1997), and also to hemoglobin and the erythrocyte membrane. The binding of lead in red blood cells may vary between spe-... 

Information on the contamination resulting from the use of anticoagulants is very scanty. Lead in heparin does not contribute significantly to the concentration of lead in whole blood, whereas for lead in plasma it does, as the concentration of lead in plasma is very low (Everson and Patterson, 1980 Cavalier and Minoia, 1981). Sodium citrate and lithium heparin were reported to contain too high concentrations of aluminium (d Haese et al., 1985), while potassium EDTA from one source - but not from another - could be used for plasma aluminium analyses (d Haese et al., 1985 Paudyn et al., 1989). Potassium EDTA from a further source was found suitable for the analysis of cobalt in whole blood (Angerer and Heinrich, 1984) however, in an analysis of a large number of trace elements, and several anticoagulants, contamination was most frequently encountered when EDTA was used (Paudyn et al., 1989). 

Blood contains lead in three forms a major fraction (about 95%) bound to erythrocytes, a protein-bound fraction in plasma, and a diffusible fraction that represents the metabolically active form of circulating blood. Since the major fraction of PbB is bound to erythrocytes, some authors have proposed expression of results in /biological validity of this correction is still controversial. With the improvement of the analytical sensitivity and reliability of the methods for measuring low levels of lead in biologicai materials, it is likely that, in future, the concentration of diffusible lead in plasma as an index of metabolically active lead will be further evaluated (Lauwerys, 1983). 

Lead is transported to the blood plasma and within minutes transferred to the erythrocytes (RBCs) and primarily bound to hemoglobin, and 6% in the plasma (Table 3). Part of the RBC lead is associated to the membrane and the remainder with hemoglobin. It is suggested that it is the diffusible lead (in plasma, where lead is bound to peptides) that produces toxic effects. Only the diffusible lead can be transported across membranes [2]. In general, lead in whole blood ranges... 

Bergdahl, I.A., Vahter, M., Counter, S.A., Schiitz, A., Buchanan, L.H., Ortega, F., et al., 1999. Lead in plasma and whole blood from lead-exposed childretL Environ. Res. 80, 25—33. 

Hirata, M., Yoshida, T., Miyajima, K., Kosada, H., Tabuchi, T., 1995. Correlation between lead in plasma and other indicators of lead exposure among lead exposed workers. Int. Arch. Occup. Environ. Health 68, 58—63. 

Smith, D., Hernandez-Avila, M., Tellez-Rojo, M.M., Mercado, A., Hu, H., 2002. The relationship between lead in plasma and whole blood in women. Environ. Health Perspect. 110, 263—268. 

Delves, H.T., Clayton, B.E., Carmichael, A., Bubear, M. and Smith, M. (1982) An appraisal of the analytical significance of tooth-lead measurements as possible indices of environmental exposure of children to lead. Ann. Clin. Biochem., 19, 329-337 Delves, H.T., Sherlock, J.C. and Quinn, M.J. (1984) Temporal stability of blood lead concentrations in adults exposed only to environmental lead. Human Toxicol, 3, 279-288 DeSilva, P.E. (1981) Determination of lead in plasma and studies on its relationship to lead in erythrocytes. Br. ]. Ind. Med., 38, 209-217... 

The volume of extracellular fluid is direcdy related to the Na" concentration which is closely controlled by the kidneys. Homeostatic control of Na" concentration depends on the hormone aldosterone. The kidney secretes a proteolytic enzyme, rennin, which is essential in the first of a series of reactions leading to aldosterone. In response to a decrease in plasma volume and Na" concentration, the secretion of rennin stimulates the production of aldosterone resulting in increased sodium retention and increased volume of extracellular fluid (51,55). 

All of the atomic species which may be produced by photon decomposition are present in plasma as well as the ionized states. The number of possible reactions is therefore also increased. As an example, die plasma decomposition of silane, SiH4, leads to the formation of the species, SiH3, SiHa, H, SiH, SiH3+ and H2+. Recombination reactions may occur between the ionized states and electrons to produce dissociated molecules either direcdy, or tlrrough the intermediate formation of excited state molecules. 

A major regulator of bone metabolism and calcium homeostasis, parathyroid hormone (PTH) is stimulated through a decrease in plasma ionised calcium and increases plasma calcium by activating osteoclasts. PTH also increases renal tubular calcium re-absorption as well as intestinal calcium absorption. Synthetic PTH (1-34) has been successfully used for the treatment of osteoporosis, where it leads to substantial increases in bone density and a 60-70% reduction in vertebral fractures. 

When carbamazepine is administered with primidone, decreased primidone levels and higher carbamazepine serum levels may result. Cimetidine administered with carbamazepine may result in an increase in plasma levels of carbamazepine that can lead to toxicity. Blood levels of lamotrigine increase when the agent is administered with valproic acid, requiring a lower dosage of lamotrigine... 

Although iron deficiency is a common problem, about 10% of the population are genetically at risk of iron overload (hemochromatosis), and elemental iron can lead to nonen2ymic generation of free radicals. Absorption of iron is stricdy regulated. Inorganic iron is accumulated in intestinal mucosal cells bound to an intracellular protein, ferritin. Once the ferritin in the cell is saturated with iron, no more can enter. Iron can only leave the mucosal cell if there is transferrin in plasma to bind to. Once transferrin is saturated with iron, any that has accumulated in the mucosal cells will be lost when the cells are shed. As a result of this mucosal barrier, only about 10% of dietary iron is normally absorbed and only 1-5% from many plant foods. 

Fig. 1.—Diagrammatic Representation of the Three Steps in the Taste-cell Transduction. Step 1, interaction of stimulus (S) with membrane-bound receptor (R) to form stimulus-receptor complex (SR) step 2, conformational change (SR) to (SR), brought about by interaction of S with R (this change initiates a change in plasma-membrane conformation of taste cells, probably below the level of the tight junction) and step 3, conformational changes of the membrane result in lowered membrane resistance, and the consequential influx on intracellular ionic species, probably Na. This influx generates the receptor potential which induces synaptic vesicular release to the innervating, sensory nerve, leading to the generator potential.

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