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© 2007 The American Society for Nutrition J. Nutr. 137:37-42, January 2007

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Molybdenum Intake Influences Molybdenum Kinetics in Men1

Janet A. Novotny2,* and Judith R. Turnlund3

2 USDA Agricultural Research Service, Beltsville Human Nutrition Research Center, Beltsville, MD 20705 and 3 USDA Agricultural Research Service, Western Human Nutrition Research Center, University of California, Davis, CA 95616

* To whom correspondence should be addressed. E-mail: janet.novotny{at}ars.usda.gov.


   ABSTRACT
TOP
 ABSTRACT
Introduction
 Methods
 Results
 Discussion
 LITERATURE CITED
 
The objectives of this study were to determine physiologic adaptations that occur when humans are exposed to a wide range of molybdenum intake levels and to identify the pathways that are influenced by dietary intake. Four males consumed each of 5 daily molybdenum intakes of 22, 72, 121, 467, and 1490 µg/d (0.23, 0.75, 1.3, 4.9, and 15.5 µmol/d) for 24 d each. During each treatment period, oral and intravenous doses of 100Mo and 97Mo were administered. Serial plasma, urine, and fecal samples were analyzed for labeled and unlabeled molybdenum. Compartmental modeling was used to determine rates of distribution and elimination at each dietary intake level. Three pathways were sensitive to daily molybdenum intake. With increasing intake, absorption and urinary molybdenum excretion increased, whereas the fraction deposited in tissues decreased. Kinetic analysis suggested a daily intake of 115–120 µg/d (1.20–1.25 µmol/d) would maintain initial plasma molybdenum levels at their prestudy values and that their prestudy dietary intake was well above the Recommended Dietary Allowance of 45 µg/d. The physiological adaptations to changing intake that the model demonstrated may help prevent molybdenum deficiency and toxicity.


   Introduction
TOP
 ABSTRACT
 Introduction
Methods
 Results
 Discussion
 LITERATURE CITED
 
Molybdenum is required in the human diet, and several enzymes found in humans contain molybdenum. These enzymes, sulfite oxidase, xanthine oxidase, and aldehyde oxidase, contain the same molybdenum complex, molybdopterine (1). Deficiency is rare in humans and is limited primarily to genetic defects leading to serious abnormalities. Deficiency symptoms in animals include retarded growth and reproductive impairments (2). Toxicity in animals and humans is more likely than deficiency, and ruminants are more susceptible to molybdenum's toxic effects than monogastric animals (3). Toxicity effects observed in animals include renal failure, reproductive effects, growth depression, and decreased hemoglobin and hematocrit. High molybdenum intakes interfere with metabolism of copper, particularly in ruminants (3). The tolerable upper intake level for the United States and Canada was set at 2 mg/d in 2002 (4), and the European Commission suggested an upper limit of 0.6 mg/d (5). Due to lack of definitive data in humans, these upper limits were extrapolated from studies demonstrating reproductive failure in rats (6). There is limited information to suggest toxicity of molybdenum to humans. Studies suggested high molybdenum intake (10–15 mg/d) contributed to hyperuricemia, symptoms of gout, and nonspecific symptoms, but these studies lacked control and follow-up (2). The lack of toxicity reports could be due to adaptations in metabolism which occur upon increasing intakes or because effects are more subtle in humans.

In this study, compartmental modeling was used to investigate changes in molybdenum distribution and elimination that occur with changing molybdenum intake. An earlier kinetic model of molybdenum metabolism with differing levels of dietary molybdenum intake was developed previously by our group (7), but the model was limited because methodology for measuring molybdenum in plasma was insufficient to provide plasma data at that time. Because plasma was the central compartment in the earlier model, the lack of plasma data hindered the ability to determine parameters of molybdenum distribution (7). Since publication of the earlier model, we developed an inductively coupled plasma mass spectrometry method that was sensitive enough to measure plasma molybdenum at the concentrations observed in our study (8). Those measurements revealed major changes in plasma molybdenum concentration due to dietary intake (9).

The newly available plasma data allowed expansion of an earlier kinetic analysis (7,10) to include the pivotal compartment of blood molybdenum. This is an important expansion to improve prediction of molybdenum flow rates and to reliably demonstrate which paths are sensitive to molybdenum intake. The expanded model was applied to data from men who were subject to a molybdenum depletion diet, followed by a molybdenum repletion period (11). The kinetic analysis suggested that a dietary intake of 43 µg/d (0.45 µmol/d) was sufficient to maintain steady state, but because clearance rates of molybdenum are dependent on dietary intake and because the analysis was based on subjects consuming a very low molybdenum diet, it was clear that this prediction could be improved by studying men undergoing a wide range of molybdenum intake levels. Thus, a kinetic study at other levels of dietary intake was needed to establish the level at which plasma molybdenum concentrations can be maintained under normal conditions and to establish which pathways change with changes in dietary intake.


   Methods
TOP
 ABSTRACT
 Introduction
 Methods
Results
 Discussion
 LITERATURE CITED
 
    Subjects, study design, treatments, and diet. The study design was described previously (12). Four healthy male volunteers participated in a study of molybdenum metabolism. Subjects' characteristics (mean ± SD) were as follows: 28 ± 5 y, 82 ± 8 kg, and BMI of 24 ± 3. Initial plasma molybdenum concentrations ranged from 8.5 to 13.8 nmol/L. All study procedures were approved by the Letterman Army Institute of Research Human Subject Review Committee and subjects gave written, informed consent prior to participation. Participants were confined to a metabolic research unit for the duration of the study. They received a low-molybdenum diet containing 22 µg/d (0.23 µmol/d) in a 3-d rotation cycle along with a molybdenum supplement beverage. The diet provided on average 11.4 ± 1.1 MJ/d, with 9% of energy from protein, 30% of energy from fat, and the remainder from carbohydrate. The base diet was supplemented with B vitamins and a beverage formula consisting of corn starch, dextrimaltose, cottonseed oil, sucrose, {alpha}-cellulose, and added salts and minerals (CaCO3, MgO, NaCl, KCl, KH2PO4, and trace elements). Energy content of the beverage varied among subjects and was calculated such that the total energy intake met the energy requirements of each subject. If a subject gained or lost weight, the amount of energy was adjusted. Diets plus supplements provided adequate levels of all essential nutrients except molybdenum. Deionized water was freely available throughout the study.

The study consisted of 5 consecutive treatment phases, with each phase being 24 d in length. The phases differed only in the molybdenum content of the diet. Dietary molybdenum levels were 22, 72, 121, 467, and 1490 µg/d (0.23, 0.75, 1.3, 4.9, and 15.5 µmol/d), starting with the lowest level for treatment period 1 and progressing to the highest level for treatment period 5. Following the first treatment phase, ammonium molybdate was added to the base diet as part of the beverage formula to achieve the desired intake level.

Stable isotope tracers were administered orally and intravenously several times throughout the study. Subjects received a 33-µg (0.34 µmol) intravenous (IV) dose of 97Mo on d 7, 55, and 103. 97Mo was delivered in solution after filtration and pH adjustment and was injected intravenously over a 2-min period. Oral doses of 100Mo were administered at the midpoint of each study period, with a tracer dose of 24 µg (0.25 µmol) on d 13, a dose of 48 µg (0.50 µmol) on d 37, a dose of 95 µg (1.0 µmol) on d 61, a dose of 428 µg (4.5 µmol) on d 85, and a dose of 1378 µg (14.3 µmol) on d 109. The 100Mo doses replaced the same mass of molybdenum in the supplement on those days, except in the first period, when no ammonium molybdenum had been added. 100Mo and 97Mo were obtained from Oak Ridge National Laboratory.

    Sample collection and analysis. During the first 24 h following each IV infusion of 97Mo, urine was collected in 8-h pooled samples. For fecal samples and all other urine samples, 6-d composite pools were collected for each subject. Blood was collected on d 1, 14, 25, 38, 49, 55, 62, 73, 86, 97, 103, 104, 110, and 121.

Molybdenum was isolated from diet, urine, and fecal samples and purified. Isotope ratios were determined in purified samples by magnetic sector thermal ionization mass spectrometry (13). Isotope ratios of molybdenum in the plasma were measured by inductively coupled plasma mass spectrometry was described previously (8). The amounts of molybdenum and isotope tracers in the samples were determined by isotope dilution by adding a weighed amount of a 94Mo solution to each weighed sample (3).

    Kinetic modeling. The WinSAAM software package was used to develop a compartmental model of molybdenum kinetics to determine which pathways, if any, were sensitive to molybdenum intake. The initial model, in which molybdenum disposition was analyzed for subjects undergoing depletion and repletion, was developed by Novotny and Turnlund (11). Initial parameter values used for fitting were averages of values reported for subjects undergoing molybdenum depletion (11). Using these parameters, model predictions were compared with measured data for tracer and tracee (100Mo, 97Mo, and total Mo) molybdenum in plasma, urine, and feces. Parameters were then adjusted in physiologically compatible ways to improve the fit of the model prediction to observed data values. The tracer and tracee data were fit simultaneously for the lowest intake level (22 µg/d) first. The resulting parameters were used to extend model prediction through the other 4 intake levels. Next, data for each intake level were fit consecutively, based on the Minimal Principle (changing the minimal number of parameters necessary to obtain sufficient fit of the data) (14). For each intake level, the model predictions for plasma, urine, and fecal 100Mo, 97Mo, and total molybdenum were compared with observed values, and this comparison was used to adjust the parameter values to improve agreement of the model prediction with the measured data. Once the model and parameters provided good visual fits for both tracer and tracee at all intake levels for all subjects, a least-squares procedure was used to minimize the difference between model prediction and observed data. Data from Rosoff and Spencer (13) were used to account for short term kinetics of labeled doses, as described previously (12).

Model parameter values across treatments were compared using a 1-way repeated measures ANOVA, and pairwise comparisons were made with a Tukey's test. Values were considered statistically different when P-values were <0.05. Statistics were performed using SigmaStat version 3.0 (SPSS).


   Results
TOP
 ABSTRACT
 Introduction
 Methods
 Results
Discussion
 LITERATURE CITED
 
The structure of the final model is shown in Figure 1. Compartments included a stomach compartment for entry of oral doses, a single gastrointestinal tract (GIT) compartment, a plasma compartment, and a tissue compartment. The tissue compartment delivered molybdenum to the gastrointestinal compartment as bile flow, and molybdenum excretion occurred as plasma delivered molybdenum to urine and the GIT delivered molybdenum to feces. Two additional compartments, specific to the infusion, were used to fit the 97Mo data, as described previously (12). One compartment was used to deliver the IV dose and the other likely represented IV molybdenum extrinsically bound to red blood cells (15,16). This model structure did not differ from that which described another group of subjects who underwent molybdenum depletion and repletion (11).


Figure 1
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  		Figure 1  Diagram of the compartmental molybdenum model. Circles show distinct kinetic compartments and arrows show pathways of flow between compartments. Dashed lines show structures that are specific to the IV dosing. Bold arrows show paths that appear to be involved in molybdenum regulation as suggested by kinetic modeling.

 
The plasma molybdenum response for a sample subject is shown in Figure 2. The measured data points are represented by symbols, and the model's prediction is represented by a line. Figure 2A shows the 100Mo content of plasma during the experiment. Figure 2B shows the 97Mo content of plasma during the experiment. Figure 2C shows total plasma molybdenum content.


Figure 2
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  		Figure 2  Plasma molybdenum response for the model prediction (line) and experimental observation (symbol) for 100Mo (A), 97Mo (B), and total Mo (C) for a sample subject. Dietary Mo levels were 22 µg/d (d 0–24), 72 µg/d (d 25–48), 121 µg/d (d 49–72), 467 µg/d (d 73–96), and 1490 µg/d (d 97–120). Change in dietary intake is marked by a dotted line. Oral doses of 100Mo (marked by arrows in A) were administered at the midpoint of each study period, on d 13 (24 µg), d 37 (48 µg), d 61 (95 µg), d 85 (428 µg), and d 109 (1378 µg). IV doses of 97Mo (marked by arrows in B) were delivered on d 7, 55, and 103. One microgram Mo = 0.0104 µmol.

 
Figure 3 shows excretion of molybdenum for a sample subject during the experiment, with circles representing observed urinary excretion, squares representing observed fecal excretion, and lines representing model prediction. The model is in good agreement with tracer excretion for both 100Mo (Fig. 3A) and 97Mo (Fig. 3B), as well as the tracee (Fig. 3C). Urine was the predominant route of excretion for the tracee and for both the oral and the IV tracer doses.


Figure 3
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  		Figure 3  Molybdenum excretion according to the model prediction (line) and experimental observation (symbol) for 100Mo (A), 97Mo (B), and total Mo (C) for a sample subject. Dietary Mo levels were 22 µg/d (d 0–24), 72 µg/d (d 25–48), 121 µg/d (d 49–72), 467 µg/d (d 73–96), and 1490 µg/d (d 97–120). Changes in dietary intake are marked by dotted lines. Oral doses of 100Mo (marked by arrows in A) were administered at the midpoint of each study period, on d 13 (24 µg), d 37 (48 µg), d 61 (95 µg), d 85 (428 µg), and d 109 (1378 µg). IV doses of 97Mo (marked by arrows in B) were delivered on d 7, 55, and 103. One microgram Mo = 0.0104 µmol.

 
Two types of parameters representing transfer of molybdenum between tissues are fractional transfer coefficients and steady-state flow rates (Tables 1 and 2). Fractional transfer coefficients represent the fraction of a compartment that travels along a given path per day. Changes in fractional transfer coefficients suggest a change in the transfer mechanism (e.g. up- or downregulation). Steady-state flow rates are the product of the fractional transfer coefficient multiplied by the steady-state mass of the donor compartment. Thus, steady-state flow rates can increase when the mass of the donor compartment increases (for example, with increased intake) without changes in the transfer mechanism. Therefore, the changes in fractional transfer coefficients are used to identify pathways for which adaptations occur.


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  		TABLE 1 Fractional transfer coefficients of molybdenum distribution for the different experimental phases1

 

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  		TABLE 2 Steady-state flow rates for molybdenum for 5 intake levels123

 
Fractional transfer coefficients for molybdenum metabolism at different intake levels are shown in Table 1. Multiplying fractional transfer coefficients by 100 converts these numbers to percent transferred per day, so, for example, movement of molybdenum from tissues to plasma had a fractional transfer coefficient of 0.13 d–1, and therefore, 13% of tissue molybdenum was mobilized into plasma per day. For the individual subjects, all parameter values were determined with good statistical certainty (fractional SDs, which reflect error associated with parameter estimates, on individual parameters below 20%). A fractional transfer coefficient value of >1 indicates that the compartment turns over more than once per day.

Three pathways were sensitive to molybdenum intake: urinary output, tissue deposition, and GIT absorption. Higher molybdenum intake resulted in higher rates of urinary excretion. Increasing dietary molybdenum intake from 22 µg/d to 72 µg/d (i.e. from 0.23 µmol/d to 0.75 µmol/d) caused a 3-fold increase in fractional transfer of molybdenum from plasma to urine, and an additional 2-fold increase was observed when subjects transitioned from 121 µg/d to 467 µg/d (from 1.3 µmol/d to 4.9 µmol/d). The deposition of plasma molybdenum into tissues was reduced at the highest molybdenum intake (1490 µg/d, or 15.5 µmol/d), but the response among subjects was highly variable. Finally, absorption efficiency was greater when higher amounts of molybdenum were present in the diet.

Based on the fractional transfer coefficients for each intake level, the model was used to calculate the steady-state flow rates and pool sizes that would result from habitual consumption of each of the 5 daily intake levels of molybdenum. Flow rates are shown in Table 2, and pool sizes are shown in Table 3. In general, increasing intakes resulted in increased flow rates and pool sizes, but because some of the pathways adapt to changing intake levels, the pattern of increase over the intake levels was not simply linear. At the highest intake level, plasma-tissue molybdenum exchange was highly variable among subjects, as evidenced by the large SDs for those flow rates. Increasing intakes of molybdenum resulted in increasing masses of molybdenum in plasma, tissues, and the GIT. Total body molybdenum ranged from 907 µg (9.43 µmol) for the lowest intake to 5421 µg (56.4 µmol) for the highest intake.


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  		TABLE 3 Steady-state pool sizes for molybdenum for 5 intake levels12

 
To fit the data for tracer (supplied partially by food-bound molybdenum) and oral tracee (supplied in supplement form) simultaneously, it was necessary to reduce the bioavailability of the food-bound molybdenum compared with that in supplement form. The model optimization calculated that the bioavailability of the food-bound molybdenum was 83% (compared with 90–94% for supplemental molybdenum).


   Discussion
TOP
 ABSTRACT
 Introduction
 Methods
 Results
 Discussion
LITERATURE CITED
 
These results have provided a number of insights into the effect of dietary molybdenum intake on regulation of molybdenum metabolism. Three pathways were sensitive to daily molybdenum intake: absorption efficiency, tissue uptake, and urinary output. The same pathways were sensitive to intake in the previous kinetic study when subjects consumed a low molybdenum diet of 22 µg/d for 102 d followed by molybdenum repletion with 467 µg/d (11). The subjects in this study were healthy young men and the responses may be different in other age groups or in women.

Urinary output appears to be the key pathway for regulating the body's exposure to molybdenum. Transitioning from 22 µg/d to 72 µg/d resulted in a tripling of the fraction of plasma molybdenum excreted into urine. Further transitioning from 121 µg/d to 467 µg/d resulted in an additional doubling of fractional transfer of plasma molybdenum into urine. Fractional transfer of molybdenum from plasma into urine did not increase further at highest level, which may suggest that the capacity for urinary excretion was exceeded. The high intake combined with the lack of increase in fractional excretion led to a substantial retention in molybdenum at the highest intake level.

Fractional uptake of molybdenum from plasma into tissues was constant for intakes below 467 µg/d but decreased by ~72% when daily molybdenum intake increased to 1490 µg. The decrease at the highest level could suggest the capacity of the tissues to store molybdenum was exceeded.

Absorption of molybdenum from the intestine increased at higher molybdenum intakes, which led to a decreased fractional transfer of molybdenum from the GIT into feces. Absorption efficiency was 90% for the lower intake levels and 94% for the higher intake levels. Increased absorption with increased intake may be due to saturation of binding of molybdenum to other food components as luminal Mo content increases.

Comparison of parameter values for the first phase of this study and the depletion phase of the previous study (11) provides insight into the effect of adaptation on molybdenum kinetics. In the depletion study, tissue deposition of molybdenum occurred more rapidly than in this study. In addition, transfer of molybdenum into the GIT via bile occurred more slowly in the previous study. Differences may be explained by the different lengths of treatment periods between the 2 studies (24 d for this study vs. 102 d for the previous study). It is likely that the subjects undergoing the shorter treatment period did not fully adapt to the intake level. The adaptation would result in conservation of tissue molybdenum during low intake.

It is likely that the tissue compartment represents predominantly liver and kidney (17). Schroeder et al. (17) reported total body molybdenum to range between 2286 and 2378 µg (~24 µmol). Our study suggested total body molybdenum to range from 907 µg to 5421 µg (9.4–56.4 µmol), depending on intake. In this study, the experimental treatment closest to estimates of free-living molybdenum intake (18,19) was 121 µg/d (1.3 µmol/d), and this intake level produced an estimate for total body molybdenum of 2224 µg (23.1 µmol), which is in good accord with the findings of Schroeder et al. (17).

The bioavailability of food-bound molybdenum was found to be lower than that for purified molybdenum. On average, the bioavailability of the food-bound molybdenum was 83%, as determined from fitting data for molybdenum in the supplement form vs. the food-bound form. Without this reduction in the bioavailability of food-bound molybdenum, plasma and urine total molybdenum were overestimated by the model and fecal total molybdenum was underestimated. Our previous kinetic analysis (11) found the bioavailability of food-bound molybdenum to be 76%, in good accord with these findings. Another study also showed that the food matrix can alter molybdenum bioavailability (20). In that study, foods were intrinsically labeled with molybdenum, and although the kale matrix did not inhibit the absorption of molybdenum, the soy matrix reduced molybdenum bioavailability by 37% compared with the purified dose.

For each set of transfer coefficients, the model was used to calculate the daily molybdenum intake that would be required to maintain plasma molybdenum at its prestudy value. For a subject in the metabolic state reflected by Phase 1 (which resulted from an intake of 22 µg/d, or 0.23 µmol/d), it would be necessary to consume 49.8 µg (0.52 µmol) molybdenum/d to maintain plasma concentrations. Because molybdenum sparing occurs at low intakes (as evidenced by the reduced transfer of molybdenum into urine for the lowest intake level compared with higher intake levels), this may underestimate the intake that would maintain baseline plasma molybdenum. For a subject in the metabolic state of Phase 2 (72 µg/d, or 0.75 µmol/d), 121 µg/d would maintain initial plasma concentrations. Compared with Phase 1, Phase 2 showed increased urinary loss; thus, this estimate is less likely to be an underestimate. For a subject in a similar state to our subjects during Phase 3 (121 µg/d, or 1.3 µmol/d), 114 µg (1.2 µmol) molybdenum/d would maintain plasma concentrations. Because this value is fairly close to the actual intake during Phase 3, then this is likely a good reflection of actual intake needed to maintain initial plasma concentrations. Further, this would suggest that the mean molybdenum intake by subjects prior to the study (thus producing the initial plasma molybdenum concentrations) was in this range. For a subject in a state similar to our subjects in Phases 4 or 5, ~270 µg (2.8 µmol) molybdenum/d would be required to maintain plasma molybdenum at the prestudy value. This higher level would be required to compensate for increased urinary losses. This analysis suggests that the molybdenum intake required to maintain initial plasma concentrations would be 115–120 µg/d (1.20–1.25 µmol/d). If one could identify a target plasma concentration based on the biological functionality of molybdenum, then a strongly justified molybdenum requirement could be calculated from this model. The value of 115–120 µg/d (1.20–1.25 µmol/d) to maintain initial plasma molybdenum concentrations is very similar to Pennington and Jones' estimate that the mean molybdenum intake of men was 109 µg/d (1.1 µmol/d) (18) and also close to the intake range of 120 to 240 µg/d (1.2 to 2.5 µmol/d) reported by Tsongas et al. (19) for molybdenum intake in the United States.

The model estimated that an intake of 115–120 µg/d (1.20–1.25 µmol/d) would maintain plasma concentrations at prestudy plasma levels, which is probably a good reflection of dietary habits prior to the study. This prediction of routine intake is substantially higher than the Recommended Dietary Allowance (4), suggesting that the usual dietary intake may generally be above the dietary molybdenum requirement. In the 2002 Dietary References Intakes, which were based on balance studies (21), a minimum requirement of 25 µg/d (0.26 µmol/d) was estimated, which was consistent with estimates for minimum requirements of several animal species (22). An average bioavailability factor of 75% was used, leading to an Estimated Average Requirement of 34 µg/d (0.35 µmol/d). To broaden the requirement to cover 97% of the population, an additional factor of 15% was added, resulting in a Recommended Dietary Allowance of 45 µg/d (0.47 µmol/d). The model suggests that the usual dietary intake is considerably higher than the dietary molybdenum requirement. The prediction that an intake of 115–120 µg/d (1.20–1.25 µmol/d) is sufficient to maintain initial plasma levels is higher than that predicted in the previous modeling analysis of men undergoing molybdenum depletion (11). The earlier prediction was lower, because it was calculated from model values of subjects in a different physiologic state.

In conclusion, these kinetic results provide a clearer understanding of the sensitivity of molybdenum disposition to differing molybdenum intakes. New insights show that several pathways adapt to molybdenum intake such that excesses are eliminated at high intakes and sparing occurs at low intakes. This reduces the risks of molybdenum deficiency and toxicity. This model also provides a means of determining dietary molybdenum intake required to maintain target plasma concentrations.


   FOOTNOTES
 
1 Supported by the USDA. Back

Manuscript received 7 June 2006. Initial review completed 10 July 2006. Revision accepted 29 September 2006.


   LITERATURE CITED
TOP
 ABSTRACT
 Introduction
 Methods
 Results
 Discussion
 LITERATURE CITED
 

1. Rajagopalan KV. Molybdenum: an essential trace element in human nutrition. Annu Rev Nutr. 1988;8:401–27.[Medline]

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5. Opinion of the Scientific Committee on Food on the Tolerable Upper Intake Level of Molybdenum. SCF/SC/NUT/UPPERLEV/22. Brussels: Scientific Committee on Food, European Commission; 2000. p. 1–15

6. Fungwe TV, Buddingh F, Demick DS, Lox CD, Yang MT, Yang SP. The role of dietary molybdenum on estrous activity, fertility, reproduction, and molybdenum and copper enzyme activities of female rats. Nutr Res. 1990;10:515–24.

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12. Turnlund JR, Keyes WR, Peiffer GL. Molybdenum absorption, excretion, and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Am J Clin Nutr. 1995;62:790–6.[Abstract/Free Full Text]

13. Turnlund JR, Keyes WR, Peiffer GL. Isotope ratios of molybdenum determined by thermal ionization mass spectrometry for stable isotope studies of molybdenum metabolism in humans. Anal Chem. 1993;65:1717–22.[Medline]

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15. Lener J, Bibr B, Kselikova M, Marik T. Peripheral membrane protein labeling of erythrocytes with 99Mo. Eur J Nucl Med. 1979;4:119.

16. Kselikova M, Bibr B, Lener J. Radioisotope (99 Mo) study of the kinetics of molybdenum clearance from the blood and of the role of blood components. Physiol Bohemoslov. 1974;23:83–8.

17. Schroeder HA, Balassa JJ, Tipton IH. Essential trace metals in man: molybdenum. J Chronic Dis. 1970;23:481–99.

18. Pennington JA, Jones JW. Molybdenum, nickel, cobalt, vanadium, and strontium in total diets. J Am Diet Assoc. 1987;87:1644–50.[Medline]

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20. Turnlund JR, Weaver CM, Kim SK, Keyes WR, Gizaw Y, Thompson KH, Peiffer GL. Molybdenum absorption and utilization in humans from soy and kale intrinsically labeled with stable isotopes of molybdenum. Am J Clin Nutr. 1999;69:1217–23.[Abstract/Free Full Text]

21. Turnlund JR, Keyes WR, Peiffer GL, Chiang G. Molybdenum absorption, excretion, and retention studied with stable isotopes in young men during depletion and repletion. Am J Clin Nutr. 1995;61:1102–9.[Abstract/Free Full Text]

22. Anke M, Groppel B, Kronemann H, Grun M. Molybdenum supply and status in animals and human beings. Nutr Res. 1985;1:S180–6.





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