Molybdenum deficiency symptoms

Peterson, N. K., and Purvis, E. R. (1961). Development of molybdenum deficiency symptoms in certain crop plants. Soil Sci. Soc. Am. Proc. 25 111-17. 

Climax Molybdenum Company (1956). Molybdenum Deficiency Symptoms in Crops. New York Climax. 

The essentiality of molybdenum for humans was determined after identification of sulfite oxidase as a molybdenum enzyme [10], the detection of a genetic deficiency of the molybdenum cofactor in a child [11,12], and the occurrence of molybdenum deficiency symptoms after molybdenum-free parenteral nutrition [13]. Apart from the genetic deficiency and the molybdenum-free parenteral nutrition, however, molybdenum deficiency does not occur in animals and humans since the general availability of molybdenum meets the requirements of animals and humans [14]. 

The antagonistic effect of tungsten was used to produce molybdenum deficiency in animals [28]. High amounts of tungsten, however, induce changes in the blood picture and diseases in cattle they do not allow their application for inducing molybdenum deficiency and disguise molybdenum deficiency symptoms [34]. 

Absorption, Metabolism, Excretion Functions of Molybdenum Deficiency Symptoms Interrelationships... 

Deficiency or Toxicity in Humans. Molybdenum deficiency in humans results in deranged metaboHsm of sulfur and purines and symptoms of mental disturbances (130). Toxic levels produce elevated uric acid in blood, gout, anemia, and growth depression. Faulty utiH2ation results in sulfite oxidase deficiency, a lethal inborn error. 

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

Molybdenum deficiency in humans has rarely been observed. The presenting symptoms included tachycardia, tachypnea, headache, night blindness, nausea, vomiting, central scotomas, lethargy, disorientation, and ultimately coma. 

Various nutrient deficiencies can affect lettuce. Boron or phosphorus deficiency causes malformed plants. Calcium deficiency causes browning of young leaves. Poor heart formation is a symptom of molybdenum deficiency. Copper deficiency prevents heads from forming. Spray seedlings with seaweed extract to help prevent nutrient deficiencies. Continue to spray plants with seaweed extract or compost tea every 2 weeks to boost plant health. Do a soil test to confirm the deficiency, and amend soil accordingly. 

Anke M, MasaokaT, Schmidt A and Arnhold W (1988) Antagonistic effects of a hi sulphur, molybdenum and cadmium content of diets on copper metabolism and deficiency symptoms in cattle andpi. In Hurley LS, et al., eds. Trace Element in Man and Animals - 6, pp. 317-318. 

A nutritional molybdenum deficiency with clinical symptoms similar to those of sulfite oxidase deficiency was identified in a human patient receiving long-term total parenteral nutrition (TPN) (Abumurad et al. 1981). The clinical symptoms included irritability leading to coma, tachycardia, tachypnea, and night blindness. A reduced intake of protein and sulfur-amino acids alleviated the symptoms, but they were aggravated by infusion of sulfite. The biochemical findings were low tissue sulfite oxidase activity a 25-fold increase in thiosulfate excretion a 70% reduction in urinary output of sulfate and a marked rise in plasma methionine. The clinical symptoms of molybdenum deficiency were totally eliminated by daily supplementation of 300 pg of the element. 

Deficiency symptoms for most micronutrients appear on the young leaves at the top of the plant, because most micronutrients are not readily translocated. Molybdenum is an exception in that it is readily translocated, and its deficiency symptoms generally appear on the whole plant. 

Symptoms of Molybdenum Deficiency Field and Horticultural Crops... 

Molybdenum deficiency in Phalaris tuberosa is manifested as pale and stunted plants with scorched and necrotic leaves, similar to those seen after frost damage (Lipsett, 1975). The symptoms appear within 3-4 weeks of seedling emergence, and subsequent growth is severely retarded. No such symptoms have been noted in conjunction with the slightly reduced growth of panic plants without Mo (Johansen, 1978a). 

The symptoms of molybdenum deficiency are usually chlorosis, yellowing of the leaves, and stunted growth (Mulder, 1950 Hewitt, 1951). These are the usual indications of nitrogen deficiency which is the result in this case of decreased nitrogen fixation, and interference with nitrogen metabolism in the cells in the absence of the activator, molybdenum. Plants seem to be able to grow normally without this element if adequate nitrogen is supplied as ammonia. 

Plants utilize molybdenum in minute amounts. The presence of one part per billion may eliminate molybdenum deficiency in plants. Evidence indicates that molybdenum plays a role in both nitrogen and phosphorus metabolism. Deficiency symptoms include an interveinal mottling with the leaf margins becoming brown. The leaf tissues wither leaving only the midrib and a few pieces of leaf blade and resulting in a characteristic appearance called whip tail (68). 

Molybdenum is considered an ultra-trace element with an approximate amount of 5 mg in the adult human body. It is a cofactor for at least three enzymes in humans (sulfite oxidase, xanthine oxidase, and aldehyde oxidase) and is involved in the catabolism of sulfur-containing amino acids, purine, and pyrimidine. A better understanding of human molybdenum metabolism is needed in order to give evidence-based recommendations regarding optimal nutrition, although molybdenum deficiency and associated pathological symptoms have not yet been observed in humans [74]. 

An adequate and safe daily dose of dietary molybdenum is 15-40 xg for children under 1 year, 25-75 p.g for children from 1 year to 6 years old and 75-250 p.g for individuals older than seven years. The actual daily dietary dose of molybdenum is in the range of about 120-240 p.g. Symptoms of molybdenum deficiency are seen mainly in farm animals that live in areas with a low molybdenum content in the soils and vegetation. 

DEFICIENCY SYMPTOMS. Naturally occurring deficiency of molybdenum in human subjects is not known, unless utilization of the mineral is interfered with by excesses of copper and/or sulfate. 

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