Aluminum blood plasma

Gardiner PE, Stoeppler M. 1987. Optimisation of the analytical conditions for the determination of aluminum in human blood plasma and serum by graphite furnace atomic absorption spectrometry. Part 2. Assessment of the analytical method. J Anal Atom Spectrom 2 401-404. 

Gardiner PE, Ottaway JM, Fell GS, et al. 1981. Determination of aluminum in blood plasma or serum by electrothermal atomic absorption spectrometry. Anal Chim Acta 128 57-66. 

Freeh. W.. Cedergren, A., Cederberg, C. and Vessman, J. (1982). Evaluation of some critical factors affecting determination of aluminum in blood, plasma or serum by electrothermal atomic absorption spectroscopy. Clin. Chem., 28, 2259. 

Subcutaneous injection of rabbits with aluminum chloride daily for 28 days was associated with significant accumulation of aluminum in bone, followed in order by significantly increased aluminum concentrations in renal cortex, renal medulla, liver, testes, skeletal muscle, heart, brain white matter, hippocampus, and plasma (Du Val et al. 1986). Because the brain tissue of treated rabbits had the lowest aluminum concentrations of the tissues evaluated, the authors suggested that there was a partial blood-brain barrier to entry of aluminum. 

Normal values of aluminum in whole blood have been reported to range from 0.14 to 6.24 mg/L (ppm), and in plasma from 0.13 to 0.16 mg/L (ppm) (Sorenson et al. 1974). Normal values in serum have been reported at 1.46 and 0.24 mg/L (ppm), using neutron activation and atomic absorption analysis, respectively (Berlyne et al. 1970). A normal value of 0.037 mg/L (ppm) for serum using flameless atomic absorption analysis has also been reported (Fuchs et al. 1974). Drablos et al. (1992) analyzed aluminum serum levels in 230 nonexposed workers (controls) and reported a mean aluminum serum level of 0.005 0.002 mg/L (ppm). Research has shown that the levels of aluminum in the serum in the general population do not exceed 0.01 mg/L (ppm) (Cornells 1982). Nieboer et al. (1995) reviewed 34 studies on aluminum levels in serum or plasma, and also reported that aluminum serum levels in the general population were typically <0.01 mg/L (ppm). 

Inductively coupled plasma-mass spectrometry (ICP-MS) is a powerful technique that uses an inductively coupled plasma as an ion source and a mass spectrometer as an ion analyzer. It can measure the presence of more than 75 elements in a single scan, and can achieve detection limits down to parts per trillion (ppt) levels for many elements—levels that are two or three orders of magnitude lower than those obtained by ICP-AES (Keeler 1991). It is more expensive than ICP-AES and requires more highly skilled technical operation. Aluminum levels in urine and saliva were detected down to 0.02 g/mL and in blood serum to 0.001 g/mL using ICP-MS (Ward 1989). Speciation studies have employed ICP-MS as a detector for aluminum in tissue fractions separated by size-exclusion chromatography (SEC) with detection limits of 0.04 g/g in femur, kidney and brain (Owen et al. 1994). 

Methods for Determining Biomarkers of Exposure and Effect. GFAAS is the method of choice for measuring low-ppb levels of aluminum in whole blood, serum, plasma, urine, and various biological tissues (Alder et al. 1977 Alderman and Gitelman 1980 Bettinelli et al. 1985 Bouman et al. 

Allain P, Mauras Y. 1979. Determination of aluminum in blood, urine, and water by inductively coupled plasma emission spectrometry. Anal Chem 51 2089-2091. 

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. 

The determination of trace metal impurities in pharmaceuticals requires a more sensitive methodology. Flame atomic absorption and emission spectroscopy have been the major tools used for this purpose. Metal contaminants such as Pb, Sb, Bi, Ag, Ba, Ni, and Sr have been identified and quantitated by these methods (59,66-68). Specific analysis is necessary for the detection of the presence of palladium in semisynthetic penicillins, where it is used as a catalyst (57), and for silicon in streptomycin (69). Furnace atomic absorption may find a significant role in the determination of known impurities, due to higher sensitivity (Table 2). Atomic absorption is used to detect quantities of known toxic substances in the blood, such as lead (70-72). If the exact impurities are not known, qualitative as well as quantitative analysis is required, and a general multielemental method such as ICP spectrometry with a rapid-scanning monochromator may be utilized. Inductively coupled plasma atomic emission spectroscopy may also be used in the analysis of biological fluids in order to detect contamination by environmental metals such as mercury (73), and to test serum and tissues for the presence of aluminum, lead, cadmium, nickel, and other trace metals (74-77). 

Aluminum salts, cholestyramine, and colestipol may decrease absorption of /3 blockers. Pheny-toin, rifampin, and phenobarbital, as well as smoking, induce hepatic biotransformation enzymes and may decrease plasma concentrations of /3 receptor antagonists that are metabolized extensively (e.g., propranolol). Cimetidine and hydralazine may increase bioavailability of propranolol and metoprolol by affecting hepatic blood flow, fi Receptor antagonists can impair the clearance o/lidocaine. 

For chronic iron intoxication e.g., thalassemia), an intramuscular dose of 0.5-1.0 g/day is recommended, although continuous subcutaneous administration (1-2 g/day) is almost as effective as intravenous administration. When blood is being transfused to patients with thalassemia, 2 g deferoxamine (per unit of blood) should be given by slow intravenous infusion (rate not to exceed 15 mg/kg/h) during the transfusion but not by the same intravenous fine. Deferoxamine is not recommended in primary hemochromatosis phlebotomy is the treatment of choice. Deferoxamine also has been used for the chelation of aluminum in dialysis patients. Deferoxamine is metabohzed principally by plasma enzymes, but the pathways have not been defined. The drug also is excreted readily in the urine. 

When the snrface of blood is protected by small thin aluminum foil, which prevents contact between blood and FE-DBD plasma but transfers all the heat generated by the plasma, no inflnence on blood is observed, which proves the non-thermal mechanism of plasma-stimnlated blood coagulation. 

Biological and clinical chemistry applications of plasma emission spectrometry include determinations of those metals required for proper functioning of living systems, such as Fe, Cu, K, Na, P, S, and Se, in urine, blood, serum, bone, muscle, and brain tissue. Aluminum exposure was suspected of playing a role in Alzheimer s disease and A1 concentrations in blood and tissue can be determined by emission spectrometry. No link between exposure to aluminum and Alzheimer s... 

After a relatively quick intake of aluminum into the intestinal walls its transition into the blood is significantly slower. In plasma aluminum is bound to approximately 80% to proteins, especially to transferrin. The amount considered currently as normal is 5 p,g/liter. Aluminum can be detected in all human organs. The only organs in which the aluminum concentration rises with progressing age are the lungs and the hilus lymphatic glands. 

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