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Plasma molybdenum concentrations were determined in children, ages two to 12 yr, with and without phenylketonuria (PKU). Mean plasma molybdenum concentrations did not differ significantly between the children with PKU (1.33 +/- 0.5 microgram/L) and without PKU (1.75 +/- 0.8 microgram/L). Plasma molybdenum concentrations in both groups of children ranged from < 1 to 3 micrograms/L. When data from all children were combined and then separated based on gender, mean plasma molybdenum levels did not differ significantly between 9 females (1.56 +/- 0.68 microgram/L) and 12 males (1.58 +/- 0.76 microgram/L). Data were also combined and mean (+/- SD) plasma molybdenum concentrations calculated for age groups. Two children aged 1 to < 4 yr had plasma molybdenum concentrations of 1.0 micrograms/L, and six children aged 4 to < 7 yr had mean (+/- SD) plasma molybdenum concentrations of 1.5 +/- 0.8 microgram/L. Eleven children aged 7 to < 11 yr had a mean plasma molybdenum concentration of 1.7 +/- 0.7 microgram/L, and two children 11 to < 14 yr had plasma molybdenum of 1 microgram/L and 2 micrograms/L. Plasma molybdenum concentrations did not differ significantly among children in the age groups.

Human red blood cells were incubated in the presence of Na2MoO4 and the initial rate of molybdenum uptake was measured by using inductively coupled plasma emission spectroscopy. About 99% of molybdenum uptake was inhibited by DIDS or by SITS. DIDS-sensitive molybdenum uptake was inhibited by external chloride, bicarbonate, sulphate and phosphate in the range of concentrations previously described for anion carrier fluxes. Trace elements, previously described to be translocated by the anion carrier, i.e. copper, zinc and cadmium, slightly inhibited molybdenum uptake. Molybdenum uptake was strongly stimulated by acidification, suggesting that the monovalent HMoO4- anion species, which is formed in acidic media (pK approximately 4.1), can be more rapidly translocated than the divalent anion complex MoO4(2-), which is the predominant form at physiological pH. In conclusion, the anion carrier can catalyse rapid molybdenum movements across red cells membranes. This supports previous reports of an enterohepatic circulation of molybdenum, with red blood cells acting as molybdenum carrier between the intestine and the liver.

Two volunteer subjects were given orally enriched solutions of Mo-95 and Mo-96 respectively. Blood samples were drawn at various times following the tracer administration. The Mo-95 and Mo-96 content in plasma samples was determined by proton nuclear activation and the response to the single oral test of enriched stable molybdenum isotopes was determined. Assuming a simple two-open-compartment model where the first compartment is the gastrointestinal tract and the other is the plasma, an indicative value of the fractional intestinal absorption for the two subjects is given. The feasibility of direct quantitative measurements of Mo intestinal absorption by the double-tracer technique, using stable tracers, is evidenced.

Though major differences exist in subcategory mortality levels, cardiovascular disease remains a leading cause of death among both Asian Chinese and Westerners. This paper examines the possible relationship between cardiovascular mortality and biochemical, diet and lifestyle factors based on two surveys in China. Statistically significant associations indicate five variables negatively correlated: molybdenum, oleic acid, liquor consumption (males), legumes, and age at first pregnancy with ischemic heart disease; molybdenum, oleic acid (females) and age at first pregnancy with hypertensive heart disease; and legumes and age at first pregnancy with stroke. Five variables were positively correlated: triglycerides and herpes antibodies with ischemic heart disease; salt and phosphorus (females) with hypertensive heart disease; and only albumin (males) with stroke. Some findings confirm those observed in the West (salt, triglycerides, herpes, legumes, oleic acid, and liquor), but molybdenum and age at first pregnancy have not been emphasized previously. Still others significant in the West have not been observed here, such as cholesterol and smoking.

We studied the dynamics of Cu, Fe, Zn, Mo, As, Cd, Pb and Se in the serum of sheep during experimental copper (Cu) intoxication from emissions from a Cu factory. From the food and the dosed emission, the daily intake was 466.8 mg Cu, 1253.93 mg Fe, 11.67 mg Zn, 0.74 mg Mo, 34.75 mg As, 0.091 mg Cd, 2.13 mg Pb, and 2.57 mg Se/experimental ewe. After the onset of Cu intoxication the first ewe died on the 65th d and the last one on the 84th d of the experiment. Hypercupremia was observed from the 50th d after the beginning of emission administration. Significant changes were observed in serum Cu on the 50th, 70th and 77th d (P less than 0.01). Changes in the dynamics of the other elements were recorded at the end of the cumulative phase and during the hemolytic crisis by also determining Fe, Zn, Mo, As, Cd, Pb and Se in serum of the Cu-poisoned sheep.

An artificial knee joint made of a cobalt alloy (Cr 27-38%, Mo 5-7%, others 9%, Co balance) failed in an orthopaedic patient with severe tissue reaction. Samples of synovial fluid and blood were analyzed for cobalt, chromium and molybdenum concentration using graphite furnace atomic absorption spectrophotometry (GFAAS). NIST SRM 909 Human Serum containing 91.3 micrograms/L chromium was used as the Cr Standard. To obtain reliable values for cobalt and molybdenum, three different independent analytical methods were employed to analyze each sample: 1) dilution of the samples with Triton TX-100 solution, followed by GFAAS; 2) microwave decomposition of the samples, followed by GFAAS; 3) classic nitric-perchloric acid decomposition of the samples, followed by GFAAS. The two decomposition methods were used to control the accuracy of the dilution method. The results showed that the non-decomposition method gave comparable results to the decomposition techniques for analysis of synovial fluid and blood. The data revealed that the patient had elevated levels of Co, Cr and Mo in both synovial fluid and blood with the values being 2-3 orders of magnitude higher in the synovial fluid from the affected knee.

The molybdenum (Mo) levels in the plasma and urine of 30 premature and 15 full-term infants have been compared with the Mo intakes and urine uric acid excretion (uric acid/creatinine ratio) produced by the Mo enzyme xanthine oxidase. The Mo intakes of full-term infants were 41 +/- 14 nmol/kg/day (mean +/- SEM). In the premature group breast milk supplied significantly less Mo (4.3 +/- 0.4 nmol/kg/day) than infant formulas (101 +/- 31 nmol/kg/day) or premature formula (255 +/- 13 nmol/kg/day). When fed breast milk, the preterm infants displayed similar or higher plasma and urine Mo and urine uric acid levels than formula-fed infants. For the whole preterm group a significant correlation was determined for urine Mo levels and Mo intakes as well as for plasma Mo and uric acid excretion. The bioavailability of breast milk Mo seems to be higher than formula Mo according to the Mo levels and to their statistical link with uric acid excretion which could be proposed as a functional index of Mo status. These parameters displayed similar values in breast milk-fed prematures and control full-term infants. The Mo needs of formula-fed premature newborns remain to be defined using complete balance trials.

The concentrations of Cd, Co, Cr, Fe, Mo, Ni, Se, Ti, V and Zn in biological fluids, human blood serum and market milk were determined by neutron activation analysis, with enrichment by coprecipitation. The pre-concentration of these trace elements was accomplished by converting the dissolved trace metal ions into their pyrrolidinedithiocarbamate (1-pyrrolidinecarbodithioate) chelates, followed by coprecipitation with a metal carrier such as Ni, Pb or Bi. The coprecipitation was carried out prior to irradiation for the short-lived nuclides (V, Ti and Se) and after irradiation for the other elements. The validity of the method was checked using certified biological reference materials; the concentrations of trace elements found by the proposed method agreed well with the published certified data. The limits of detection for Cd, Co, Cr, Fe, Mo, Ni, Se (obtained through the long-lived isotope 75Se) and Zn under the present experimental conditions were found to be 5, 5, 10, 520, 5, 70, 10 and 150 ng, respectively, for 5 ml of biological liquor. The limits of detection for Ti and V obtained (through their short-lived radionuclides 51Ti and 52V, respectively) were found to be 180 and 1.4 ng, respectively, for 50 ml of market milk, or 70 and 0.7 ng for 1 ml of blood serum.

Examination of direct and (Cu)-difference spectra of i) the aqueous supernatants of in vitro cultures of bovine rumen contents incubated with MoO42- and potential sources of S2- and ii) samples drawn directly from the rumen of animals receiving high Mo diets yielded evidence of the presence of thiomolybdates. Only MoS42- was detected in the soluble phase of in vitro cultures. Although intense and variable background absorbance precluded full characterization of thiomolybdate species in samples drawn directly from the rumen, both spectral data and the biochemical and clinical responses of animals given high Mo diets were consistent with the conclusion that MoS42- rather than MoOS32- was the predominant thiomolybdate species present in the aqueous phase. Addition of Ca2+ either to rumen cultures before incubation or as a supplement to diets high in MoO42- content inhibited the appearance of MoS42- in the aqueous phase. Evidence of the sequestration of MoS42- and MoOS32- by particulate or microbial fractions of rumen contents is considered in relation to the inhibitory action of Mo upon Cu absorption by ruminants.

An initial experiment showed that [99Mo]di- and trithiomolybdates could be detected in bovine plasma after the introduction of [99Mo]molybdate into the rumen. It was felt that this justified the use of [99Mo]trithiomolybdate for the subsequent studies made of plasma thiomolybdate metabolism in vivo in cattle. Rapid intravenous injection of [99Mo]trithiomolybdate into cattle showed that doses of 50 mg Mo were subject to extensive hydrolysis over the first few minutes postinjection, but at lower dose rates this was reduced so that tracer doses (less than 1.5 mg Mo) were relatively stable. The plasma metabolism was unaffected by copper status within the limits of the experiments (that is, liver copper levels down to 9 mg/kg d.m.) The disappearance of [99Mo] and [35S]trithiomolybdate (1 mg Mo) from plasma was delayed for up to 10 hr by the immediate preinjection of copper, although no chemical modification of the thiomolybdate appeared to occur.

1. The ability of organic and inorganic sulphur to influence the copper and molybdenum metabolism of sheep was compared in a series of three 2 X 2 factorial design experiments. In each experiment, four groups of five to seven hypocupraemic ewes were repleted with a basal diet supplemented with 6 mg Cu/kg and containing S and Mo at one of two concentrations, 1 or 4 g S and 0-5 or 4-5 mg Mo/kg respectively. Sodium sulphate (Expt I), methionine (Expt 2) or cysteine (Expt 3) were used as the S sources. Cu and Mo concentrations in plasma were estimated in each experiment and in Expt 3 the concentrations of Cu in liver and Mo in urine were also estimated. 2. The effects of the three S sources on Cu and Mo metabolism were similar. Repletion of the plasma Cu pool was unaffected by Mo alone, reduced by S alone and totally inhibited by Mo+S. Plasma Mo was greatly increased by Mo supplements, slightly decreased by S supplements and unaffected by Mo and S supplements given together. 3. In Expt 3 the treatments were found to affect urinary Mo and plasma Mo in a similar manner; S prevented dietary Mo from increasing Mo excretion. The only group to show a significant repletion of the liver Cu pool was that given Mo alone. 4. Supplementation of the diet with organic S significantly reduced the within-treatment variation in plasma Cu and Mo. liver Cu and urinary Mo. 5. It is suggested that variations in dietary S and Mo within the normal range for herbage affect the Cu and Mo metabolism of the grazing animal, and that total S rather than inorganic S is the more useful measurement in the context of the Cu-Mo-S interrelationship.

The absorption of labelled molybdenum compounds was studied in pairs of sheep exchanging digesta via re-entrant duodenal cannulae. Tri- and tetrathiomolybdate 99Mo were rapidly absorbed from the rumen to circulate in plasma in a protein-bound and in a TCA-insoluble form. The compounds were also absorbed from the small intestine although some breakdown was evident. Initially, molybdate was poorly absorbed from the rumen but after several hours the concentration of protein-bound, TCA-insoluble 99Mo increased in plasma. This provides evidence of rumen thiomolybdate synthesis. The results indicate that thiomolybdates are absorbed directly from the rumen and despite the sensitivity of the compounds to acid, some absorption from the small intestine occurs after passage through the abomasum. Rumen absorption could be a contributory factor to ruminant sensitivity to the effects of Mo compounds.

As one of a series of studies on the influence of S substitution of MoO4(2-) on the action of Mo as an antagonist of Cu, the effects of MoO2S2(2-) and MoOS3(2-) on the metabolism of Cu by rats have been investigated. Administration of either oxythiomolybdate increased both plasma Cu concentration and the retention of Cu by the albumin fraction of plasma. In contrast to the effects of MoS4(2-), described previously, neither oxythiomolybdate inhibited 64Cu absorption from the digestive tract or induced biochemical or clinical signs of Cu deficiency. Evidence is discussed suggesting that the potency of the thio- and oxythiomolybdates as inhibitors of Cu utilization is directly proportional to the degree of thio substitution within the series series MoO4- chi S chi 2-.

Several investigators have reported serum molybdenum determinations in healthy humans. However, their results diverge quite widely. We determined the element by neutron activation analysis in 30 individuals. We found a mean value of 0.58 ng/ml, a standard deviation of 0.21 ng/ml and a range of 0.28--1.17 ng/ml.

On separate occasions young cattle were injected intrarumenally with 99Mo or 64Cu or intravenously with 64Cu. The metabolism of the isotopes were compared to evaluate metabolic changes associated with molybdenum-induced copper deficiency. Molybdenum-99 metabolism was the same in both controls and experimental subjects. Marked differences in plasma kinetics were observed following intrarumenal 64Cu injection, with experimental animals displaying earlier plasma appearance and maintaining higher plasma levels than did controls. Similarly, higher plasma levels, more rapid plasma reappearance and greater fecal excretion were observed following intravenous injection of 64Cu in the experimental animals than in controls. A mechanism involving abnormal ceruloplasmin synthesis associated with the molybdenum-copper interaction is proposed.

1. Protein-bound, trichloracetic acid- (TCA) insoluble 99Mo appeared in plasma a few hours after the introduction of 99Mo-labelled molybdate (30 mg Mo) into the rumen of sheep maintained on a basic diet supplemented with elemental sulphur (3 g S/d). 2. Most of the 99Mo could be displaced from its protein carrier in vitro and the labelled compounds displaced were identified by sephadex G-25 chromatography as di- and trithiomolybdate. Tetrathiomolybdate was not detected. 3. In control experiments protein-bound, TCA-insoluble 99Mo predominated in plasma after the direct administration of [99Mo]tetrathiomolybdate, either into the rumen or intravenously. The 99Mo could be displaced in vitro and [99Mo]tetrathiomolybdate identified, although [99Mo]trithiomolybdate was also present. The study provides direct evidence of thiomolybdate synthesis and absorption in ruminants in vivo.

A sensitive method is described for the determination of Mo in plasma or serum by graphite furnace atomic absorption spectrometry. The method involves extraction of the metal as the 8-hydroxyquinoline complex and is free of the interference effects that prevent the direct analysis of plasma for Mo. Recoveries of internal standards were excellent and results from the analysis of a National Institute of Standards and Technology Standard Reference Material were in good agreement with certified values. The sensitivity of the method, based on the analysis of 1 ml of plasma, is ca. 3 ng ml-1.

Studies were carried out on the content of micro and macroelements in the fodder and cattle blood serums. Haematocrit and haemoglobulin were estimated in full blood. The results underwent statistical analysis and arithmetical means, standard deviation, essential differences and correlations were calculated among the studied features. There was a low content of calcium and magnesium in the fodder. Decreased levels of copper and magnesium were found in the blood serum. Depending on the keeping of cattle and season of the year essential differences and correlations were noted among the studied features.

1. At 16 h after the rapid injection of 99Mo-labelled compounds into the rumen of sheep maintained on dried grass (6.2 mg molybdenum/kg dry matter (DM), 4.3 g sulphur/kg DM), labelled thiomolybdates associated with the digesta solids or bound to plasma macromolecular species were displaced from their carriers in vitro and identified by Sephadex G25 chromatography. 2. After molybdate injection, the thiomolybdates displaced from rumen, duodenal and ileal solids were predominantly the trithio- and tetrathio- species. Dithiomolybdate was present to a relatively minor extent. Trace amounts of di- and trithiomolybdates were detected in the liquid phase of digesta from the duodenum. 3. Whether injected into the rumen as molybdate or tetrathiomolybdate, bound 99Mo appearing in plasma was present mainly as di- and trithio- species. The tetrathio- species appeared in trace amounts in plasma only after tetrathiomolybdate injection, despite its existence almost exclusively in this form in rumen digesta. 4. The present study provides direct evidence for thiomolybdate synthesis within the rumen and indicates that while the effects of thiomolybdates in inhibiting copper absorption are likely to be due to tri- and tetrathiomolybdates, post-absorptive effects on Cu metabolism are probably due to di- or trithiomolybdate.

The effect on Cu metabolism of two organic Mo compounds, cysteine-Mo (CM) and cysteine-Mo-S (CMS), and of an inorganic compound, tetrathiomolybdate (TTM), was investigated in sheep. Intravenous administration of CMS or TTM increased total plasma Cu concentrations and promoted the appearance of trichloroacetic acid (TCA)-insoluble Cu in plasma. Plasma Mo was increased by both compounds. Column chromatography of plasma showed that CMS caused the accumulation of TCA-insoluble Cu in high-MW fractions, whereas TTM increased the Cu content of low-MW fractions, mainly albumin. CMS and TTM increased the concentration of Cu and Mo in kidney. In liver, Mo concentrations were elevated by both CMS and TTM, and Cu concentrations were reduced by TTM when it was given at a low dose rate. The subcellular distribution of Cu and Mo in liver and kidney was investigated. The findings are discussed in relation to the proposal that Mo-containing, organic compounds are intermediaries in the interaction between Cu, Mo, and S in ruminants.

Spectral studies showed that copper and trithiomolybdate participated in a three-way interaction with bovine and canine serum albumin. The interaction with the proteins was affected by increased pH and ionic strength. Kinetic studies of binding equilibria indicated that [35S] trithiomolybdate bound to both albumins at a single site. The affinity of the site, but not the capacity of the protein, was increased by copper. It was concluded that the site was distinct from the N-terminal copper (and nickel) binding site, which is present on BSA but absent from CSA. Whether or not the N-terminal site has a role in copper transport is discussed. Reversible thiomolybdate-copper-protein interactions of this type may play a fundamental role in the pathogenesis of Mo-induced syndromes, since as the normal binding patterns are perturbed the interprotein equilibria are altered and the copper distribution patterns are modified.

Sheep were infused intravenously with 99Mo- and 35S-labelled tri- and tetrathiomolybdates (1-2 mg Mo). Most of the plasma radioactivity was trichloroacetic acid (TCA)-insoluble after infusion, but the stability of this fraction was reduced by pre-infusion or subsequent infusion with unlabelled thiomolybdates. Most of the 99Mo and 35S was shown to be associated with albumin. It was concluded that compounds bound to albumin were relatively stable, but displaced or unbound thiomolybdates were rapidly hydrolysed to molybdate and sulphate. There was no evidence of an irreversible interaction of either 35S or 99Mo with copper in plasma, despite the appearance of a TCA-insoluble Cu fraction. Increased dietary Cu did not increase the retention of 35S in plasma or affect the exchangeability of 36S-labelled thiomolybdates bound to albumin.

Calves were fed milk replacer containing 10, 50, 200, 500, or 1000 ppm Cu, from 3 d to 45 d of age, to estimate the Cu concentration that would adversely affect calf performance. Weight gains and feed efficiency were similar for 10 and 50 ppm Cu but were reduced at 200 and 500 ppm Cu. All calves survived 500 ppm Cu and lower intakes, but only 4 of 7 calves survived the 1000 ppm concentration. Typical clinical symptoms of chronic Cu toxicity and hemolytic crisis were evident for the 1000 ppm calves before death. Additional 1000 ppm Zn prevented deaths for 1000 ppm Cu, but calf performance was poor. Increased Cu intakes elevated plasma ceruloplasmin and glutamic oxalacetic transaminase activity, reduced packed cell volume (hematocrit), markedly increased fecal excretion of Mo and Zn, increased Cu concentration of liver, muscle, heart, blood, and bile, and decreased Mo and Zn in liver. We found 50 ppm Cu a safe intake where milk replacer contained 48 ppm Zn and 1.1 ppm Mo. However, at lower intakes of these elements, and for longer feeding periods than 6 wk, the calf may be much more susceptible to Cu toxicity.

A pyrolytic carbon coating was applied to F-75 chromium-cobalt-molybdenum alloy in an effort to reduce the release of corrosion products in vivo. After intramuscular implantation in the rat, a complex pattern of serum and urine concentration elevations of chromium, cobalt, and nickel was seen. The carbon-coated implants released more chromium and cobalt than uncoated controls, as seen by significantly elevated metal concentrations in serum and urine. Animals receiving carbon-coated implants showed a high rate of recurrent implant site inflammation. Neoplastic infiltration of 24 animals with coated implants, but not in any of the 16 animals which received either uncoated F-75 microsphere or poly(ethylene) particulate implants.

We determined the serum molybdenum concentration by neutron activation analysis in apparently healthy subjects and in patients with diseases of the liver and biliary system. The level was found to be markedly elevated in the initial phase of acute viral hepatitis (mean +/- S.D. 3.10 +/- 1.46 ng/ml vs. 0.55 +/- 0.21 in controls) and to return to normal during convalescence, in parallel with the liver function tests. The most significant correlations were found between the serum molybdenum concentration and the serum levels of GOT ( r = 0.710, p less than 0.001) and GPT (r = 0.683, p less than 0.001). Besides, the serum molybdenum level (mean +/- S.D.) was observed to be definitely increased in patients with HBsAg-positive chronic active hepatitis (0.97 +/- 0.49 ng/ml), HBsAg-positive liver cirrhosis (1.01 +/- 0.50), alcoholic liver disease (1.32 +/- 0.56), liver metastases (1.40 +/-0.39), gallstones (1.28 +/- 0.38), tumors of the gallbladder or extrahepatic bile ducts (1.64 +/- 0.44), and carcinoma of the head of the pancreas (1.61 +/- 0.91). Finally, the serum molybdenum level was found to be raised in two patients with primary biliary cirrhosis and in two out of four patients with drug-induced liver injury. The etiologic mechanism and the clinical importance of the observed abnormality remain to be established. Our study enlarges the existing information concerning the disorders of trace element metabolism in liver diseases.

After incubating plasma of Mo-supplemented rats (Mo-plasma) with 64Cu only part of it could be removed by dialysis against EDTA or histidine or by treatment with dithiocarbamate; this nondialyzable Cu was shown to be bound to albumin. The maximal amount of 64Cu bound this way equaled the Mo-induced increase in total plasma Cu. After addition of stable Cu, dialysis of Mo-plasma against a histidine solution showed that no extra Cu became tightly bound, suggesting that the 64Cu binding was due to an exchange between added 64Cu and stable Cu already present. Incubating Mo-plasma with Hg compounds prevented 64Cu binding and released stable Cu, indicating that Cu in Mo-plasma was sulfhydryl bound. Part of the Mo in Mo-plasma was freely dialyzable. The remaining part was shown to be SH bound as well. The estimated atomic ratio of SH-bound Cu and Mo was unity. Molybdenum increased the number of SH groups in plasma, and for each Cu atom at least one SH group was calculated to be present.

The elements Ag, Au, Cd, Co, Cr, Cs, Mo, Rb, Sb, and Se were determined in platelets from seven normal donors. The results, in ng/g wet weight, for plasma-free platelets follow: "Pure" platelets: Ag = 29 +/- (18), au = 0.22 +/- (0.22), Cd = 6.2 +/- 3.4, Cs = 54.8 +/- 19.2, Cr = 6.1 +/- 2.5, Co = 7.5 +/- (5.0), Mo = 3.4 +/- 1.3, Rb = 10400 +/- 3000, Sb = 18 +/- (26), and Se = 782 +/- 127. "Impure" platelets: Au = 0.23 +/- (0.28), Cd = 6.4 +/- 2.6, Cs = 35.2 +/- 13.8, Cr = 8.2 +/- 2.9, Co = 2.9 +/- (3.0), Mo = 3.2 +/- 0.8, Rb = 8700 +/- 1700, Sb = 13.2 +/- (8.7), and Se = 679 +/- 57. To our knowledge, none of these 10 trace elements has been determined in platelets before. The selenium concentration in platelets exceeds that in other tissues (e.g., liver). We suggest that glutathione peroxidase or other unknown selenoenzymes are particularly important in platelet metabolism. Platelets are crucial for triggering thrombosis, and so may be involved as links between selenium deficiency and the concomitant increased death rate from cardiovascular disease.

Exposure to molybdenum in dust was measured in a molybdenite roasting plant. This exposure was accompanied by large elevations of serum ceruloplasmin and smaller increases in mean serum uric acid levels in the workers. Absorption of molybdenum from the dust was demonstrated by increases in plasma and urinary molybdenum levels. It remains necessary to demonstrate whether such exposure results in long-term health effects.

The radioactive labeling of spectrin using the pentavalent complex of molybdenum-99 was applied to the study of membrane protein in pyruvate kinase deficient red cells. Compared to the control, the labeling profile of the enzymopathic red cell membrane proteins remained generally unchanged but the molybdenum uptake was found to depend largely on the reticulocyte count. This finding may reflect changes during the cell maturation.

Molybdenum (Mo), selenium (Se) and copper (Cu) plasma levels were studied at delivery in 38 women (1 twin pregnancy). The influence of parity (P) (2.5 +/- 1.7) gestational age (GA) (38.6 +/- 3.2 weeks), birthweight (BW) (3,120 +/- 695 g) and Apgar score upon these levels were assessed. Mother (M) and cord (C) blood values were 15.0 +/- 7.8 and 15.0 +/- 9.3 nmol/l respectively for Mo, 0.54 +/- 0.12 and 0.47 +/- 014 mumol/l for Se and 27.6 +/- 5.9 and 5.5 +/- 3.3 mumol/l for Cu. C and M values for Se and Cu were statistically different (alpha less than 0.02, alpha less than 0.001). There was a significant correlation between C and M for Mo levels (r = 0.41; p = 1.9%) and Cu levels (r = 0.47; p = 0.35%), between Cu C levels and GA (r = 0.54; p = 0.6%) and between Se, C levels and BW (r = 0.66; p = 1.9%). There was no correlation between the levels of the trace elements studied. This study shows that fetal levels of Mo vary with those of the mothers. On the other hand, the levels of Se in the fetus seem to be protected from variations observed in the mothers. The antagonism between Cu and Mo which had been previously demonstrated in the fetal liver was not found in blood.

The effects of molybdenum ingestion on copper metabolism were investigated in bile duct-cannulated ponies fed diets containing 1.01, 27.4 and 107.3 ppm molybdenum. Copper metabolism was assessed by examination of 64Cu and stable copper excretion in feces, bile and urine. The addition of molybdenum to the diet decreased copper absorption and retention as a consequence of increased excretion of dietary copper in feces and increased excretion of absorbed copper in bile. Only 5% or less of the absorbed copper was excreted in urine regardless of dietary treatment. Biliary molybdenum excretion was only 0.86 mg per 100 kg of body weight per day even when ponies were fed the highest level of molybdenum. However, increased molybdenum ingestion produced elevations in protein bound copper in bile. Molybdenum was absorbed by ponies but urinary excretion was effective in eliminating most of the element from the body.

1. A 30-week study has been made in growing ewe lambs of the effects of dietary supplementation with molybdenum, or Mo plus inorganic sulphate on the distribution of copper in their blood plasma and kidneys. 2. The addition of 25 mg Mo and 5 g SO42-/kg diet increased Cu concentrations in plasma and kidney and decreased those in liver. Plasma caeruloplasmin activities (ferroxidase; EC 1.16.3.1) were unaffected. 3. Subcellular fractionation of the kidney cortex and gel filtration of the plasma and kidney cortex cytosol showed that the increased Cu content of these tissues was associated with abnormalities in the distribution of Cu. It appeared that both Cu and Mo were associated with the same proteins. 4. Dietary supplementation with Mo alone (25 mg/kg) had no effect on plasma or kidney Cu concentrations, suggesting that S metabolism is involved in the formation of the abnormal Cu-binding proteins in plasma and kidney. 5. The results are discussed in relation to the induction of Mo-induced Cu-deficiency states and the possible involvement of thiomolybdates.

A method is presented for determining molybdenum in plant tissue and blood plasma by flame and flameless atomic absorption spectroscopy (AAS). The samples are digested with HNO3-HCIO4, and the metal is separated by chelation, extracted into methyl isobutyl ketone, and analyzed by AAS. Recoveries of molybdenum from fortified samples ranged from 92.0 to 98.9%. The limits of detection on the flame and graphite furnace were 10 and 2 ng/mL, respectively.