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Journal of Veterinary Diagnostic Investigation Vol. 18 Issue 6, 566-572
Copyright © 2006 by the American Association of Veterinary Laboratory Diagnosticians
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Full Scientific Reports

Modest copper supplementation blocks molybdenosis in cattle

Merl F. Raisbeck1, Roger S. Siemion and Michael A. Smith

Correspondence: 1Corresponding Author: Merl F Raisbeck, 1174 Snowy Range Rd, Laramie, WY 82070


   Abstract
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 Abstract
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It is widely accepted that ratios of dietary copper (Cu) to molybdenum (Mo) lower than 10:1 may produce molybdenosis in cattle, especially if sulfur concentrations are more than 3,000 ppm. Some authorities suggest that dietary Mo concentrations greater than 10 ppm are hazardous to cattle regardless of Cu concentration, but anecdotal reports suggest that this may not be the case. The original purpose of the experiment described in this report was to investigate whether supranutritional supplemental Cu could protect cattle against relatively high dietary Mo. Pregnant cows were grazed on 1 of 3 pastures: 1 with only background Mo, 1 with an average of 13 ppm Mo, and 1 that averaged 230 ppm Mo. Half the cows on the Mo pastures were supplemented with 17 ppm dietary Cu, the other half with the dietary supplement plus Cu boluses. Molybdenum effects were anticipated in the groups supplemented with 17 ppm Cu; however, despite increased tissue concentrations of Mo, only the 230 ppm Mo/17 ppm Cu group exhibited any effects. Moderate Cu supplementation permitted cows to graze a site heavily contaminated with Mo with no adverse effects on general health or reproduction.

Key Words: Ceruloplasmin • copper • molybdenum • pregnancy • superoxide dismutase • tissue concentrations


   Introduction
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 Abstract
 Introduction
Materials and Methods
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As a result of natural or anthropogenic (eg, mining, manufacturing) processes, molybdenum (Mo) may become sufficiently concentrated in soil and vegetation to cause molybdenum poisoning (molybdenosis) in grazing cattle.12 The toxic effects of Mo result from copper (Cu) deficiency5 at both the whole animal (pharmacokinetic)3,12,13,17,22 and cellular level.2,4,10 Sulfur (S) potentiates most, if not all, of the effects of Mo in ruminants. Sulfide, which is formed in the rumen, displaces the oxygen in molybdate, forming various thiomolybdates that react with Cu at several levels, reducing both the dietary uptake1 and biological availability of Cu to the cell.9,19 The ratio of Cu, Mo, and S in the diet is critical to the Cu-Mo-S interaction and thus toxicity. A dietary ratio of 2:1 Cu:Mo is regarded as the absolute lower limit of acceptable diets for cattle, although many authorities insist that 10:1 is necessary.9,11,13,21

Because of these interactions, the specific combination(s) of Cu, S, Mo, and other dietary factors that pose a hazard under field conditions are difficult to determine with precision and seem to vary considerably with location. Much of the older literature suggests that 5–10 ppm dietary Mo is invariably hazardous to cattle, regardless of Cu concentrations, but recent reports describe cattle grazing higher concentrations with no adverse effects, especially when given adequate Cu supplementation under arid rangeland conditions.6–8,20,21 The experiment described in this report was carried out between November 1999 and October 2000 in a large (approximately 2023 hectare [ha]) pasture in northern Utah that had been contaminated with Mo as a result of burning industrial wastes during the previous decade and was reported to frequently produce molybdenosis in cattle. The purpose of the experiment was to determine if moderate or supranutritional Cu supplementation could block or ameliorate the toxic effects of relatively high dietary Mo forages in beef cattle.


   Materials and Methods
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The contaminated pasture was divided on the basis of previous years' forage and soil data into a small (approximately 121 ha) enclosure with extremely high (up to 930 ppm) Mo concentrations (the "burn site") and a much larger (approximately 1,902 ha) area where Mo concentrations were projected, on the basis of analyses of previous years, to be approximately 20 ppm (the "pasture"). A third pasture with similar terrain and vegetation approximately 10 miles distant (the "ranch") served as a control. The predominant forage species on all three sites were cheatgrass (Bromus tectorum), dropseed (Sporobolus airoides), tall wheatgrass (Agropyron sp.) and salt grass (Distichalis spicata). Transects (1 on the burn site, 4 on the pasture, and 2 on the ranch) were established in representative areas of each site ,and representative forage samples were taken at intervals (200 m, except on the burn site, where they were approximately 100 m) by clipping all edible vegetation more than 10-cm tall in a 1-m2 area into a paper bag. Samples were air dried to constant weight, ground to 60 mesh, and mixed before subsampling and analysis (Table 1).


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  		Table 1 Forage molybdenum concentrations (µg/g dry weight).

 
Through the cooperation of a local rancher, 600 head of pregnant beef cows were studied between November 1999 and October 2000. All cattle were maintained on a basal diet of pasture and free-choice trace mineral salt containing 750 ppm Cu in accordance with the owner's normal practices. Before the experiment, all cattle were weighed and pregnancy tested. From the whole herd, the 306 most closely matched cattle were ranked according to body weight, pregnancy status, and age. From that ranking they were randomly assigned to 1 of 5 treatment groups: Group I consisted of 3 cows (positive controls) pastured on the burn site; Group II consisted of 3 cows pastured on the burn site, like Group I, but receiving 25 g of supplemental Cu as a bolusa every 60 days; Group III consisted of 123 cows grazed on the pasture; Group IV consisted of 118 cows also grazing the pasture with Group III but receiving Cu boluses every 60 days; and Group V, the control group, was 59 cows pastured at the ranch. Subgroups of 30 animals apiece were similarly selected from within Groups III, IV, and V for more intensive monitoring, including tissue and blood sampling.

Cows were introduced to the test pastures in mid-December 1999. Bulls (approximately 1 per 25 cows, except at the burn site, which received only 1 bull) were turned in with all cows on the following May 15 and rotated in accordance with the owner's normal procedures. After the winter-spring grazing/calving trial, all cattle were moved to their usual summer pastures in Idaho on June 14, 2000. At this time all 5 groups were comingled to eliminate effects of any discrepancy between summer pastures. Cows were pregnancy checked, and cows and calves weighed again at weaning after returning from summer range in mid-October 2000.

Trace-element supplements were prepared on the basis of projected forage conditions. Because trace-element salt consumption had been poor in previous years, compressed block supplement "tubs,"b designed to be consumed at 0.45 kg/head/day, were provided free choice. The tubs provided on the pasture and on the burn site (Groups I through IV) were formulated to provide 17 ppm supplemental Cu (ie, above that provided by forage) on a total dietary basis. Identical tubs, supplying approximately 2 ppm supplemental Cu, were provided to the control group at the ranch. In addition, as noted previously, cattle in Groups II and IV were given Cu boluses every 60 days to determine if supranutritional supplementation was of benefit.

During February and March, the poor quality of available forage necessitated supplemental feeding. Alfalfa hay was fed at approximately 18 kg/head on alternate days (to encourage cows to continue foraging the local grass) from February 1 to February 21 on all 3 sites. After February 21, pregnant cows were fed 10.45 kg/head/day until they calved. Most cows were off supplemental hay by early March. The last date that any hay was fed was March 21.

Body weight and condition score were evaluated before and after the grazing trial, at monthly intervals while animals were on site and at the end of the summer grazing season. Calves were weighed at birth, when the herd left for summer pasture, and when weaned before shipping in fall 2000. At the beginning and end of the experimental grazing period, liver biopsies were collected by percutaneous biopsy and analyzed for Cu, Mo, iron (Fe), and zinc (Zn) on a dry-weight basis. Blood was collected into a variety of containers each time the cattle were weighed. Heparinized samples were refrigerated for 24 to 72 hours until assayed for superoxide dismutase (SOD) or were frozen for Mo analysis. Serum was harvested from clot tubes for ceruloplasmin assays and frozen until assayed. Serum from trace-element grade tubes was frozen until assayed for Cu, Mo, Fe, and Zn. Ethyleneaminetetraacetic acid (EDTA) blood was refrigerated until complete blood counts could be performed (usually 24 hours). Any cow showing signs of illness during the experiment was captured and given a thorough physical examination by a licensed veterinarian. The same veterinarian likewise subjected any cow that died to postmortem examination.

Ceruloplasmin was assayed by standard methods16 at Kansas State University College of Veterinary Medicine Department of Diagnostic Medicine/Pathobiology. Superoxide dismutase was assayed in erythrocytes using a commercial kit,c and the results were normalized to hemoglobin concentration. Complete blood counts were performed on an automated readerd by the Wyoming State Veterinary Laboratory Clinical Pathology Laboratory. Samples for trace-element analysis (eg, serum, liver) were ashed with concentrated HNO3 and 37% H2O2 in a microwave unit.e Trichloracetic acid (TCA)–soluble Cu was determined in serum by precipitating the protein with 5% TCA and analyzing the supernatant. Trace-element analyses were performed on either an ARL 3520 ICP-OESf or an Elan 6100 ICP/MSg in the Wyoming State Veterinary Toxicology Lab. Each analytic run included external standards and matrix-matched reference samples.h The criterion for acceptance of an analytic run was reference sample concentrations within 10% of nominal.

Quantitative data were analyzed by analysis of variance (ANOVA) or ANOVA with repeated measures using a commercial microcomputer program.i Post hoc comparisons were performed where appropriate by the Bonferroni test. Weaning weights were normalized to 205 days for statistical analysis. Pregnancy rates were compared between groups by chi-square analysis with the same program. Because of their small size, Groups I and II were excluded from statistical analysis unless otherwise specifically noted. A P value of 0.05 was used to determine significance unless otherwise noted.


   Results
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 Abstract
 Introduction
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 Results
Discussion
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Although each group experienced the illnesses and losses typical of range cattle (eg, dystocia, respiratory infections), only 2 cattle, both in Group I, showed clinical signs consistent with molybdenosis during the last 2 weeks of the experiment. These consisted of persistent, watery, gassy diarrhea and lameness. Because the regular veterinarian was not available, a local veterinarian who was not familiar with the experiment examined both cattle. The bull was diagnosed as having a spinal injury on the basis of a visual examination and was treated symptomatically with flunixin meglumine.j The cow was diagnosed as having a bacterial infection on the basis of an elevated white blood count (22,900/mm3) with neutrophilia (72%) and many band cells (14%) and was treated with tetracycline.k Serum Mo was slightly elevated in the bull (0.12 ppm) and markedly elevated in the cow (3.38 ppm). Total serum Cu was 1.3 ppm in both. Clinical signs abated within a week without further treatment and the animals involved were sound (ie, pregnant and with viable semen) the following year.

Early in the experiment (January 2000) the researchers discovered that crude protein values in forage ranged from 3% to 4% on all sites. This is insufficient to support cattle in late pregnancy and necessitated supplemental feeding in the form of alfalfa (1.4 ppm Cu, 5 ppm Mo) to all groups. Once forage began to turn green, forage protein concentrations increased to 10% to 20%, and supplemental feeding was discontinued. Forage Mo concentrations were greatest in the burn site (Groups I and II) with some samples exceeding 900 ppm (average 230 ppm) (Table 1). Pasture (Groups III and IV) Mo concentrations ranged from 5 to 23 ppm (average 13 ppm) and ranch (Group V) forage contained less than 2 ppm (Table 1). Forage Cu concentrations were similar (P< 0.05) between all sites and increased from approximately 2 ppm at the beginning of the experiment (December 1999) to 10 to 20 ppm with the coming of green grass (mid March). Iron and Zn remained within adequate dietary limits throughout the grazing trial.

There were no significant differences between groups in cows' mean body-weight change (ie, gain or loss) or condition score during the grazing trial, or again when calves were weaned at the end of the summer (data not shown). Likewise, there was no difference between treatment groups in the mean birth weight of calves, the mean body weight of calves at the end of the grazing trial, or the 205-day adjusted weaning weight when calves were sold in the fall (Table 2). There were no statistically significant differences between Groups III, IV, and V in blood packed cell volume, mean corpuscular hemoglobin concentration, total red blood cell counts, white blood cell counts, or lymphocyte counts, and the mean values of all groups remained within normal clinical limits during the study (data not shown).


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  		Table 2 Calf weights at birth, on June 14, 2000, and at weaning the next fall.*

 
As might be expected, liver Mo concentrations showed a dramatically (P<0.001) greater increase between December and June in Groups I and II than in the other 3 groups (Fig. 1). The increases in Groups III and IV (3.4 ± 1.9 ppm and 3.0 ± 2.0 ppm, respectively) were not significantly different from the slight gain seen in Group V (2.4 ± 1.8 ppm), there were no significant differences between Groups III, IV, and V in the June 2000 liver Mo concentrations (6.73 ± 1.99 ppm, 6.44 ± 2.0 ppm, and 5.36 ± 1.49 ppm, respectively); however, Groups III and IV included more animals in the diagnostic range (> 6 ppm, 17 in each) than did the control group (n = 3).


Figure 18060701
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  		Figure 1 Increased hepatic Mo (ppm dry matter) while on contaminated pasture. Data are presented as the mean change in hepatic Mo concentration (± standard error) between December 1999 and June 2000. Superscripts indicate statistical similarity.

 
Liver Cu increased in all 5 groups between December and June (Fig. 2). Not surprisingly, the increase was significantly greater (P<0.001) in Group IV than in either Groups III or V. Group III, grazed on the pasture with 17 ppm supplemental Cu from blocks, did not differ significantly from the control cows (Group V) at the ranch. Liver Zn declined in all groups (data not shown), but the magnitude of the decrease did not differ significantly between groups, and the decline did not result in concentrations that were outside clinical normal limits (120 to 400 ppm dry weight). Hepatic Fe concentrations were not clinically significant, and they were not significantly different between groups after the grazing trial (data not shown).


Figure 18060702
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  		Figure 2 Mean hepatic Cu increase (ppm dry matter) while on Cu supplementation. Data are presented as the change in hepatic Cu concentration (mean ± standard error) between December 1999 and June 2000. Superscripts indicate statistical similarity.

 
Total serum Cu concentrations increased in Groups I and II (the burn site) relative to Groups III, IV, and V. There were no significant differences in total serum Cu between the other 3 groups throughout the study (data not shown). Measures of TCA-soluble serum Cu were slightly but nonsignificantly greater at the end of the grazing period in Group IV (Cu bolus) than in the controls (Group V) or Group III (without boluses). The TCA-soluble serum Cu concentration was greater in Groups I and II (the burn site) than in the other 3 groups by 67 days and continued to increase until the end of the season (Fig. 3). Mean serum Mo concentration were increased in Groups I through IV relative to the control group. By 67 days, mean Mo in Groups I and II (burn site) were significantly greater than levels in Groups III, IV, and V, and this pattern continued until the end of the grazing trial (Fig. 4). Serum Mo concentrations were also greater in Groups III and IV (pasture) than in Group V (controls) during this period. Blood Mo concentrations paralleled serum Mo concentrations (data not shown), and both blood and serum peaked slightly around the first of May on the high levels of Mo, but not the control or pastures, and the concentrations declined thereafter. This peak followed the growth of new forage by 30 to 45 days.


Figure 18060703
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  		Figure 3 Concentration of TCA-soluble serum Cu. Data are presented as mean µg/ml ± standard error. Superscripts indicate statistical similarity.

 

Figure 18060704
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  		Figure 4 Serum Mo concentration. Data are presented as mean µg/ml ± standard error. Superscripts indicate statistical similarity.

 
There were no significant differences between groups in serum Fe, Zn, ceruloplasmin, or SOD activity at any point during the grazing period (data not shown). There was, however, a trend to lower SOD activity in Group I on the burn site without boluses (data not shown). This is consistent with the fact that 1 cow and 1 bull in this group showed transient clinical signs (eg. diarrhea) consistent with molybdenosis. These symptoms resolved in a couple of weeks without any intervention, and all Group I animals were clinically normal at the end of the experiment.

There were more open (nonpregnant) cows at weaning in the control group (12%) than in either group on the Mo pasture (6% to 7%) (Table 3); however, these differences were not statistically significant. According to the owner, his herd averages about 8% to 10% open cows in a typical year. The open rate for his entire herd, including cattle not involved in the experiment, was 11% for this particular year. All of the Group I cows and 2 of 3 Group II cows were pregnant at the end of the year.


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  		Table 3 Cross-tabulation analysis of pregnancy status at weaning.*

 
On the premise that Mo might have caused subclinical effects that were not readily reflected in any of the parameters measured, the economic loss of cows and calves because of all causes was compared between groups. Counting a cow that began the experiment in December 1999 and was absent or open at weaning the following October as "lost," Group III lost 6%, Group IV lost 5%, and Group V lost 5%. The difference between groups was not significant (P<0.867). Calf production was analyzed in a similar fashion. From the 306 cows in the experiment, 287 calves were turned out to summer pasture (Table 4). At weaning, 10 calves, although present and in good health, could not be used in the statistical analysis because they lost their ear tags. There was no significant difference between groups, either when all 5 groups were included in the analysis or when only Groups III, IV, and V were compared.


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  		Table 4 Cross-tabulation analysis* of calf survival among calves born on the high Mo pasture.

 

   Discussion
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 Sources and manufacturers
 Abstract
 Introduction
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 Results
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References
 
With the exception of the bull and cow in Group I, no cattle exhibited any of the typical signs of molybdenosis/copper deficiency, and the difference in dietary Mo was not reflected in weight gain or loss or lower body condition score at the end of the trial grazing period or at weaning. Whether the 2 animals were suffering from simple molybdenosis is uncertain as the local veterinarian who examined them was unfamiliar with molybdenosis and did not collect the correct samples, but it seems likely that Mo was a factor, especially in the cow. Serum Mo concentrations were markedly elevated when she was examined and SOD activity (3.97 units/ml) was more than 2 standard deviations less than the controls (5.23 ± 0.53 units/ml) when all cattle were moved to summer pasture approximately a week later.

In theory, molybdenosis causes subclinical effects (eg, immunosuppression) that might not be manifested for several months; however, there was no evidence of subclinical effects at weaning as reflected in total mortality or loss of pregnancy due to all causes. Although cattle on the burn site were not included in most statistical analyses because of the very small numbers involved, it is interesting that all of the Group I cows were pregnant at the end of the year. In contrast, the only Group II cow open at the end of the year was delivered of 36.4 kg twins while on the burn site and was in very poor condition as a result.

Not surprisingly, liver Mo concentrations were significantly increased in Groups I and II, relative to the control group. Serum Mo concentrations in Groups I through IV increased more than controls and showed a small, statistically insignificant peak around the first of May on the high Mo sites, but not on the control pasture. This peak followed growth of new forage by 30 to 45 days but the significance of the relationship is uncertain. The peak may reflect seasonal variation in forage Mo concentrations or pharmacokinetic redistibution of the Mo body burden. Unfortunately, an insufficient number of forage analyses were performed to determine which was the case. Surprisingly, hepatic Mo concentrations also increased somewhat through the grazing season in Group V. This probably reflects differences between the ranch and the previous summer/fall pasture; however, only 2 of the Group V cows were in the diagnostic range (>6 ppm) described by other authors,14,15,18 and 17 were elevated above diagnostic concentrations in each of Groups III and IV. In addition, all of the serum Mo concentrations in Groups III and IV were elevated into a range (>0.1 ppm) considered to be diagnostic of molybdenosis14 by the first of May, whereas none of Group V were at any time. Interestingly, none of the Group III or IV animals showed any clinical, biochemical or production evidence of toxicosis.

Total serum Cu concentrations were increased in groups on the Mo-contaminated sites. This is expected in ruminants with molybdenosis as much of the serum Cu is tied up in a biologically unavailable form.10,21 What is surprising, however, is that TCA-soluble serum Cu was also greater in cattle exposed to very high Mo on the burn site (Groups I and II) by 67 days and continued to increase until the end of the season. Although the numbers of animals were very small, and none of the Cu results were outside of physiologic norms, TCA-soluble Cu should decrease in cattle on high-Mo diets as biologically unavailable forms of Cu are precipitated by TCA.10 This unexpected result may reflect greater mineral (block) consumption by the burn site cattle, but the difference in measured consumption between all groups was only about 20%. Thus, it appears that there may be some as yet undefined physiologic factors at very high dietary Mo intakes that result in increased TCA-soluble serum Cu.

The only biochemical indication of excessive Mo intake was a trend to lower SOD activity in Group I (burn site, no boluses). Because SOD reflects an essential physiologic function of Cu rather than merely its presence, it is an excellent marker of Cu adequacy and, indirectly, Mo toxicity. This trend in Group I (extremely high Mo, moderate Cu) is consistent with the fact that 1 cow and 1 bull in this group showed transient clinical signs (diarrhea) compatible with molybdenosis. Given the history of molybdenosis on this pasture for several years and the high forage Mo concentrations present during the experiment, the researchers assumed that providing modest Cu supplementation would not be sufficient to overcome the effects of elevated dietary Mo in Group III; thus, a supranutritional dietary Cu group (IV) was included, which would presumably demonstrate any benefits from supranutritional Cu supplementation. However, relatively conventional Cu supplementation (17 ppm) of the basal diet overcame the effects of Mo in cattle on the pasture (Group III) without the additional Cu provided by the boluses, despite serum and liver Mo concentrations diagnostic of molybdenosis.12,14 Although the degree of supplementation given Group III is slightly greater than the National Research Council (NRC) minimum requirements,13 the practice is common in Cu-deficient areas, and the researchers anticipated discovering significant differences in biochemical or production parameters between Groups III and IV as a result of supranutritional supplementation with boluses. There were, however, none. It is also possible that low forage S concentrations lessened the impact of Mo. Although forage S was not analyzed as part of this experiment, historical S concentrations on the sites, taken over several years, were only 0.01% to 0.1%. Sulfur is a critical part of the Cu-Mo interaction,1,9,11,21 and it is possible that if forage S was significantly greater Mo effects would have been seen in Group III.

Cattle grazing elevated Mo forage accumulated greater amounts of tissue and serum Mo compared to cattle grazing a similar control site. Despite several year's history of molybdenosis on this pasture, and serum and liver Mo concentrations elevated to a range purportedly diagnostic of molybdenosis,14,15,18 none of the cows in Groups III or IV exhibited any adverse effects because of Mo, either while on the pasture or at the end of their production year when calves were weaned. This is most likely the result of providing adequate, but not excessive (or supranutritional), Cu supplementation.

There is a tendency to rely heavily on mineral concentrations in a limited number of forage, tissue, or serum mineral analyses to diagnose trace-element deficiencies or intoxications. If a limited number of samples yield results that are "high," "toxic," or "marginally deficient" compared to a published range, the case is closed and therapy instituted without doing more extensive sampling or evaluating the bigger picture. This study, the largest known of its type, demonstrates that forage Mo concentrations and tissue (17/30) and serum (30/30) Mo concentrations (in Groups III and IV) considered to be within "toxic" ranges do not necessarily prove that molybdenosis has occurred.


   Sources and manufacturers
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Abstract
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From the Department of Veterinary Sciences (Raisbeck, Siemion) and the Department of Renewable Resources (Smith), University of Wyoming, Laramie, WY. Back

a. Copasure-25, Schering Plough Animal Health, Union Hill, NJ. Back

b. Key Lix, Winn Feed, Smithfield, UT. Back

c. SOD-525, Oxis Corp, Portland, OR. Back

d. QBC Autoread Hematology Analyzer, IDEXX Corp, Westbrook, ME. Back

e. MDS 2000 Microwave Digestor, CEM Corp, Raleigh, NC. Back

f. ARL 3500, Advanced Research Labs, Sunland, CA. Back

g. Elan 6100, Perkin Elmer, Norwalk, CT. Back

h. NIST, Gaithersburg, MD. Back

i. SYSTAT, SPSS Corp, Chicago, IL. Back

j. Banamine, Schering-Plough Animal Health, Kenilworth, NJ. Back

k. LA200, Pfizer, Groton, CT. Back


   References
TOP
 Sources and manufacturers
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Allen J.D., Gawthorne J.M.: 1987, Involvement of the solid phase of rumen digesta in the interaction between copper, molybdenum and sulphur in sheep. Br J Nutr 58:265–276.[Medline]
  2. Arthington J.D., Corah L.D., Blecha F.: 1996, The effect of molybdenum induced copper deficiency on acute-phase protein concentrations, superoxide dismutase activity, leukocyte numbers and lymphocyte proliferation in beef heifers inoculated with bovine herpesvirus-1. J Anim Sci 74:211–217.[Abstract]
  3. Bailey J.D., Ansotegui R.P., Paterson J.A., et al.: 2001, Effects of supplementing combinations of inorganic and complexed copper on performance and liver mineral status of beef heifers consuming antagonists. J Anim Sci 79:2926–2934.[Abstract/Free Full Text]
  4. Cerone S., Sansinanea A., Streitenberger S., et al.: 1998, Bovine neutrophil functionality in molybdenum-induced Cu deficiency. Nutr Res 18:557–566.
  5. Ferguson W.S., Lewis A.H., Watson S.J.: 1938, Action of molybdenum in nutrition of milking cattle. Nature 141:553 pp.
  6. Gardner W., Broersma K.: 1999, Cattle grazing high molybdenum pasture on reclaimed mine tailings. In: Molybdenum issues in reclamation: Proceedings of British Columbia Mine Reclamation Symposium. pp. 66–75. British Columbia Technical and Research Committee on Reclamation, Smithers, BC, Canada.
  7. Gardner W.G., Quinton D.A., Popp J.D., et al.: 1997, The use of copper boli for cattle grazing high-molybdenum forage. In: Toxic plants and other natural toxicants, ed Garland T., Barr A., pp. 115–119. CAB International, London.
  8. Gardner W.C., Broersma J.D., Popp J.D., et al.: 2003, Copper and health status of cattle grazing high molybdenum forage from a reclaimed mine tailing site. Can J Anim Sci 83:479–485.
  9. Gooneratne S.R., Buckley W.T., Christensen D.A.: 1989, Review of copper deficiency and metabolism in ruminants. Can J Anim Sci 69:819–845.
  10. Lannon B., Mason J.: 1986, The inhibition of bovine ceruloplasmin oxidase activity by thiomolybdates in vivo and in vitro: a reversible reaction. J Inorg Biochem 26:107–115.[Medline]
  11. Miltmore J., Mason J.: 1971, Copper to molybdenum ratio and molybdenum and copper concentration in ruminant feeds. Can J Anim Sci 51:193–200.
  12. National Research Council: 1980, Molybdenum. In: Mineral tolerance of domestic animals. pp. 328–344. National Academy Press, Washington, DC.
  13. National Research Council: 2000, Nutrient requirements of beef cattle, 7th ed. pp. 54–64. National Academy Press, Washington, DC.
  14. Puls R.: 1994, Mineral levels in animal health: diagnostic data, 2nd ed. pp. 192–199. Sherpa International, Clearbrook, BC, Canada.
  15. Swan D.A., Creeper J.H., White C.J., et al.: 1998, Molybdenum poisoning in feedlot cattle. Aust Vet J 76:345–349.[Medline]
  16. Tietz N.W.: 1982, Fundamentals of clinical chemistry. pp. 270–271, 296, 346, 584, 649–652, 923. WB Saunders, Philadephia, PA.
  17. Underwood E.J.: 1976, Molybdenum in animal nutrition. In: Molybdenum in the Environment, ed Chappel W.R., Petersen K.K., pp. 9–30. Marcel Dekker, New York.
  18. US Fish and Wildlife Service: 1989, Molybdenum hazards to fish, wildlife and invertebrates: a synoptic review. US Fish and Wildlife Service Biological Report 85 (1.19). US Fish and Wildlife Service, Washington, DC.
  19. Wang Z.Y., Poole D., Mason J.: 1988, The effects of supplementation of the diet of young steers with Mo and S on the intracellular distribution of copper in liver and on copper fractions in the blood. Br Vet J 144:543–551.[Medline]
  20. Ward G.M.: 1991, Acceptable limits of molybdenum for ruminants exist. Feedstuffs 14:15–22.
  21. Ward G.M.: 1994, Molybdenum requirements, toxicity and nutritional limits for man and animals. In: Molybdenum: an outline of its chemistry and uses, ed Braithwaite E.R., Haber J., pp. 452–576. Elsevier, Amsterdam.
  22. Ward J.D., Spears J.W.: 1999, The effect of low-copper diets with or without supplemental molybdenum on specific immune responses of stressed cattle. J Anim Sci 77:230–237.[Abstract/Free Full Text]




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