Urine molybdenum

There is about 0.5 p,g Mo per L (5nmol/L) in plasma or serum and about l Llg Mo per L (lOnmol/L) in whole blood. Urine molybdenum values determined by ICP-MS vary from 40 to 60 pg/L, the amount determined being influenced by recent dietary intake. ... 

About 50% of copper in food is absorbed, usually under equitibrium conditions, and stored in the tiver and muscles. Excretion is mainly via the bile, and only a few percent of the absorbed amount is found in urine. The excretion of copper from the human body is influenced by molybdenum. A low molybdenum concentration in the diet causes a low excretion of copper, and a high intake results in a considerable increase in copper excretion (68). This copper—molybdenum relationship appears to correlate with copper deficiency symptoms in cattle. It has been suggested that, at the pH of the intestine, copper and molybdate ions react to form biologically unavailable copper molybdate (69). 

Devoto 115)has described an indirect procedure for the determination of 0.1 ppm arsenic in urine. The arsenomolybdic acid complex is formed and extracted from 1 ml of urine at pH 2 into 10 ml of cyclohexanone. The molybdenum in the complex is then measured. Before extracting the arsenic, phosphate in the urine is separated by extracting the phosphomolybdic acid complex at pH 1 into isobutyl acetate. The direct determination of arsenic in biological material and blood and urine is best done using a nitrous oxide-acetylene flame 116>. The background absorption by this flame is low at 1937 A, and interferences are minimized due to the high temperature of the flame. 

Several investigators have described the indirect determination of orthophosphate by extraction of the phosphomolybdic acid complex and the measuring the molybdenum extracted. Zaugg and Knox 2921 first applied this technique to the determination of phosphate in urine. A protein-free filtrate was formed and the complex was extracted into 2-octanol. More recently, Devoto 293) determined 0 to 25 pg of phosphate in 50 ml of urine by extracting the complex from acidified urine into isobutyl acetate. 

Workers at a molybdenum-roasting plant with time-weighted average (TWA) exposures of approximately 9.5mgMo/m to soluble dusts had increased plasma and urine levels of molybdenum the only adverse biochemical findings were large elevations in serum ceruloplasmin levels and some increase in serum uric acid levels. ... 

Organ meats, legumes and grains are good sources. The adequate range of molybdenum intake for adults is 75 to 250 meg/day. It is equally excreted in the urine and the faeces. 

Electron density calculations suggest that electrophilic attack in pyridine (42) is favored at C-3, whereas nucleophilic attack occurs preferentially at C-2 and to a lesser extent at C-4. Cytochrome P-450 mediated ring hydroxylation of pyridine would, therefore, be expected to occur predominantly at C-3, the most electron-rich carbon atom. Although 3-hydroxypyridine is an in vivo metabolite in several species, the major C-oxidation product detected in the urine of most species examined was 4-pyridone (82MI10903). The enzyme system catalyzing the formation of this latter metabolite may involve the molybdenum hydroxylases and not cytochrome P-450 (see next paragraph). In the related heterocycle quinoline (43), positions of high electron density are at C-3, C-6 and C-8, while in isoquinoline (44) they are at C-5, C-7 and C-8. Nucleophilic substitution predictably occurs... 

The evidence for a pterin-substituted 1,2-enedithiolate was first reported by Raja-gopalan, Johnson, and coworkers, who isolated pterins from the oxidative decomposition of molybdenum-bound MPT, Figure 4 [7,49,55,56], In complementary work, Taylor and coworkers confirmed the structure of several of the pterin decomposition products by direct synthesis (see Section V. A) [30,57-59], Urothi-one, first isolated in 1940 from human urine [60], was shown to be a metabolic degradation product of MPT [37], Other isolated pterin-containing decomposition and/or derivatized products from molybdenum enzymes include Form A, Form B (a urothione-like product), and camMPT (Figure 4) [7], Two other pterins, Form Z and the MPT precursor, can be obtained from molybdenum deprived organisms, N. crassa Nit-1, and oxidase-deficient children, neither of which pro-... 

Elevated levels of chromium in blood, serum, urine, and other tissues and organs have been observed in patients with cobalt-chromium knee and hip arthroplasts (Michel et al. 1987 Sunderman et al. 1989). Whether corrosion or wear of the implant can release chromium (or other metal components) into the systemic circulation depends on the nature of the device. In one study, the mean postoperative blood and urine levels of chromium of nine patients with total hip replacements made from a cast cobalt-chromium-molybdenum alloy were 3.9 and 6.2 pg/F, respectively, compared with preoperative blood and urine levels of 1.4 and 0.4 pg/F, respectively. High blood and urinary levels of chromium persisted when measured at intervals over a year or more after surgery. These data suggest significant wear or corrosion... 

The modeling and ultimate total synthesis of molybdopterin and Mo-co have been hampered by difficulties associated with the pterin chemistry involved. However, synthetic assaults on molybdopterin, the molybdenum cofactor, and the degradation products of the molybdenum cofactor are now well underway. The total chemical synthesis of urothi-one (7), the postulated metabolic excretory product of Mo-co (25), has recently been reported (4 7). Compound 7 is a naturally occurring substituted thiophene that is found in the urine of normal humans. It is absent (25) from the urine of children who lack the molybdenum cofactor due to a genetic defect and who are unable to metabolize sulfite (48). The absolute configuration of Form A (8), another degradation product of... 

Molybdenum is very efficiently absorbed, in contrast, for example, to copper and iron. With doses of 0-025—1,4 mg Mb, only 1% of the mineral is recovered in the feces. With a single dose of a low level of the mineral (<0.025 mg), about 20% of the mineral is recovered in the urine during a 6collection period. With a large test dose (1.4 mg), about 90% of the dose is recovered in a six day period (Tumlund et fli., 1995). 

A procedure for the determination of molybdenum in serum, red blood cells, and urine is described. The low concentration of molybdenum in most unexposed individuals requires the sensitivity obtained using atomic absorption spectrophotometry and electrothermal atomization. Spike recovery tests indicate that low temperature ashing is required for accuracy. Severe matrix interferences preclude wet ashing or high-temperature ashing as sample pretreatments. Using the method described, it is possible to distinguish between industrially exposed and unexposed individuals. 

Biological fluids such as serum or plasma, red blood cells, and urine are particularly diflBcult to analyze. The low molybdenum concentrations found in normal human samples are below the detection limit of the thiocyanate colorimetric method (100 ng) and much below conventional flame absorption spectroscopy (1 /xg). Normal blood levels of molybdenum are about 10 /xg/L and sample volume is usually < 1 mL. The low concentration and limited sample size preclude direct analysis or sample preconcentration for analysis by the conventional analytical methods. 

In summary, a method for the analysis of molybdenum in biological fluids has been presented. The method requires the destruction of the organic materials in the sample by low-temperature ashing. Detection was accomplished by using a graphite furnace—atomic absorption technique and the standard additions method. The method is sufficiently sensitive to distinguish between molybdenum levels in the blood, serum, and urine from exposed and unexposed individuals. 

Molybdenum is efficiently absorbed over a wide range of dietary intakes mainly as molybdate, although competitive inhibition of absorption by sulfate reduces intestinal uptake. Concentrations in whole blood are about l.Opg/L (10 nmol/L) and some 80% to 90% or more of molybdenum in whole blood is bound to red cell proteins. Transport of the smaller amount in blood plasma may involve a2-macroglobulin. Urine output directly reflects the... 

Iversen BS, Menne C, White MA, Kristiansen J, Christensen IM, Sabbioni E. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Analyst 1998 123 81-5. 

One common way to determine phosphorus in urine is to treat the sample, after removing the protein, with molybdenum(VI) and then reduce the resulting 12-molybdophosphate complex with ascorbic acid to give an intense blue-colored species called molybdenum blue. The absorbance... 

The single-point standard addition method was used in the determination of phosphate by the molybdenum blue method. A 2.00-mL urine sample was treated with molybdenum blue reagents to produce a species absorbing at 820 nm, after which the sample was diluted to 100 mL. A 25.00-mL aliquot of this solution gave an absorbance of 0.428 (solution 1). Addition of 1.00 mL of a solution containing 0.0500 mg of phosphate to a second 25.0-mL aliquot gave an absorbance of 0.517 (solution 2). Use these data to calculate the concentration of phosphate in milligrams per milliliter of the specimen. 

A calibration curve for the colorimetric determination of phosphorous in urine is prepared by reacting standard solutions of phosphate with molybdenum(VI) and reducing the phosphomolybdic acid complex to produce the characteristic blue color. The measured absorbance A is plotted against the concentration of phosphorous. From the following data, determine the linear least-squares line and calculate the phosphorous concentration in the urine sample ... 

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