# molybdenum information from California.



## hay wilson in TX (Jan 28, 2009)

Molybdenum Deficiency in Alfalfa Production










Author: Rachael Freeman Long
April 11, 2013



There have been several alfalfa fields in the Northern Sacramento Valley area that have been deficient in molybdenum (Mo or moly), which is unusual, but not unheard of for the Sacramento Valley. Symptoms of molybdenum deficiency are like those of nitrogen and sulfur deficiency: light green or yellow, stunted plants, caused by a lack of moly that is essential for nitrogen fixation by the rhizobium bacteria that live on alfalfa roots. There may be a region just south of Sacramento that may have alfalfa with somewhat low concentrations of Mo but as you go further south, Mo toxicity begins. Some low copper-high molybdenum soils have been documented in the Modesto and south areas.

Plant tissue testing is the only way to confirm a molybdenum deficiency. Collect samples from the top 6-inches or one-third of a plant, or from whole plant samples collected from baled hay. Plant samples with less than 0.3 ppm are considered deficient, 0.4 to 1.0 ppm marginal, 1 to 5 ppm adequate, and 5 to 10 ppm high. Concentrations over 10 ppm may be toxic to livestock. High moly concentrations in alfalfa should be offset with copper concentrations that are twice as high as molybdenum concentrations to prevent livestock toxicity.

The most common moly fertilizer is sodium molybdate (40% molybdenum), but ammonium molybdate can be used as well. Follow the label carefully and apply during winter or before re-growth has resumed after cutting. Broadcast on the soil surface only and avoid application to any plant foliage. A single application of 0.4 pounds per acre of molybdenum should last from 5 to 15 years. Thorough records of molybdenum application times and amounts along with repeated tissue testing are essential to determine when to apply or reapply this nutrient.

Do not apply excessive molybdenum (that is double or triple coverage with the sprayer at the end of the field) because the concentration of the element in alfalfa may become so high that the forage becomes toxic to livestock. For the same reason, do not apply molybdenum directly on foliage. Analyzing the top one-third of the plant for both copper and molybdenum can detect deficiencies and suboptimum ratios of these elements in forages.

Deficiency often occurs on slightly acid to very acid soils. Increasing the soil pH increases solubility and availability of soil molybdenum.


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## hay wilson in TX (Jan 28, 2009)

More Moly information

Molybdenum

Most molybdenum compounds have low solubility in water, but the molybdate ion MoO42− is soluble and forms when molybdenum-containing minerals are in contact with oxygen and water. Industrially, molybdenum compounds (about 14% of world production of the element) are used in high-pressure and high-temperature applications, as pigments and catalysts.

Molybdenum-containing enzymes are by far the most common catalysts used by some bacteria to break the chemical bond in atmospheric molecular *nitrogen*, allowing biological *nitrogen fixation*. At least 50 molybdenum-containing enzymes are now known in bacteria and animals, although only bacterial and cyanobacterial enzymes are involved in nitrogen fixation, and these nitrogenases contain molybdenum in a different form from the rest. Owing to the diverse functions of the various other types of molybdenum enzymes, molybdenum is a required element for life in all higher organisms (eukaryotes), though not in all bacteria.

Copper-molybdenum antagonism

High levels of molybdenum can interfere with the body's uptake of copper, producing copper deficiency. Molybdenum prevents plasma proteins from binding to copper, and it also increases the amount of copper that is excreted in urine. Ruminants that consume high amounts of molybdenum develop symptoms including diarrhea, stunted growth, anemia and achromotrichia (loss of hair pigment). These symptoms can be alleviated by the administration of more copper into the system, both in dietary form and by injection.[74] The condition, as an effective copper deficiency, can be aggravated by excess sulfur.[32][75]

Copper reduction or deficiency can also be deliberately induced for therapeutic purposes by the compound ammonium tetrathiomolybdate, in which the bright red anion *tetrathiomolybdate* is the copper-chelating agent. Tetrathiomolybdate was first used therapeutically in the treatment of copper toxicosis in animals. It was then introduced as a treatment in Wilson's disease, a hereditary copper metabolism disorder in humans; it acts both by competing with copper absorption in the bowel and by increasing excretion. It has also been found to have an inhibitory effect on angiogenesis, potentially via the inhibition of copper ion dependent membrane translocation process involving a non-classical secretion pathway.[76] This makes it an interesting investigatory treatment for cancer, age-related macular degeneration, and other diseases featuring excessive blood vessel deposition.[77][78]

Copper-molybdenum antagonism

High levels of molybdenum can interfere with the body's uptake of copper, producing copper deficiency. Molybdenum prevents plasma proteins from binding to copper, and it also increases the amount of copper that is excreted in urine. Ruminants that consume high amounts of molybdenum develop symptoms including diarrhea, stunted growth, anemia and achromotrichia (loss of hair pigment). These symptoms can be alleviated by the administration of more copper into the system, both in dietary form and by injection.[74] The condition, as an effective copper deficiency, can be aggravated by excess sulfur.[32][75]

Copper reduction or deficiency can also be deliberately induced for therapeutic purposes by the compound ammonium tetrathiomolybdate, in which the bright red anion *tetrathiomolybdate* is the copper-chelating agent. Tetrathiomolybdate was first used therapeutically in the treatment of copper toxicosis in animals. It was then introduced as a treatment in Wilson's disease, a hereditary copper metabolism disorder in humans; it acts both by competing with copper absorption in the bowel and by increasing excretion. It has also been found to have an inhibitory effect on angiogenesis, potentially via the inhibition of copper ion dependent membrane translocation process involving a non-classical secretion pathway.[76] This makes it an interesting investigatory treatment for cancer, age-related macular degeneration, and other diseases featuring excessive blood vessel deposition.[77][78]


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