Molybdenum: Quality Detoxification
Molybdenum (Mo)
For humans – qualitative detoxification.
In the human body molybdenum acts as a cofactor in enzymes responsible for detoxifying the body, influences the utilization of iron stores in the body, activates the metabolism of sulfur-containing amino acids, which are important for the functioning of the nervous system and brain, helps retain fluoride in the body, strengthening tooth enamel and protecting them from decay.
The daily requirement for the human body is 75–250 µg, and for individuals over 75 years old – 200 µg. Some authors believe that the daily requirement for molybdenum is about 0.3–0.4 mg.
Molybdenum from food sources and in the form of soluble complexes is easily absorbed. In humans, 25–80% of molybdenum from food is absorbed. Absorption occurs in the stomach and throughout the small intestine, more so in its proximal part than in the distal part. The absorption of molybdenum is significantly influenced by interactions between molybdenum and various dietary forms of sulfur.
Then about 80% of the molybdenum that enters the bloodstream binds to proteins (primarily albumin) and is transported throughout the body. In the blood, molybdenum is evenly distributed between formed elements and plasma. Most of the molybdenum quickly enters the kidneys and is excreted by them. Excretion is the main mechanism of its homeostatic regulation. Significant amounts of this element are excreted with bile. Accumulation of molybdenum does not occur in the bodies of mammals.
Organs containing high amounts of molybdenum are the liver and kidneys.
Organs containing high amounts of molybdenum are the liver and kidneys.
Biological role in the human body. The physiological significance of molybdenum for the bodies of animals and humans was first demonstrated in 1953, with the discovery of the influence of this element on the activity of the enzyme xanthine oxidase, which is responsible for purine metabolism (xanthine oxidase facilitates the conversion of purines into uric acid). Molybdenum promotes more efficient functioning of antioxidants, particularly vitamin C. It is an important component of the tissue respiration system. It enhances amino acid synthesis and improves nitrogen accumulation.
Molybdenum is part of several enzymes (aldehyde oxidase, sulfite oxidase, xanthine oxidase, etc.) that perform important physiological functions, particularly regulating uric acid metabolism.
Molybdenum enzymes catalyze the hydroxylation of various substrates. For example, aldehyde oxidase oxidizes and neutralizes various pyrimidines, purines, and pteridines. Xanthine oxidase catalyzes the conversion of hypoxanthine to xanthines, and xanthines to uric acid (with increased xanthine oxidase activity in the blood, excessive uric acid accumulates, leading to gout). Sulfite oxidase catalyzes the conversion of sulfite to sulfate.
Molybdenum deficiency in the body is accompanied by a decrease in xanthine oxidase content in tissues. In molybdenum deficiency, anabolic processes are impaired, and there is a weakening of the immune system. Ammonium thiomolybdate (a soluble molybdenum salt) acts as a copper antagonist and disrupts its utilization in the body. There is evidence that molybdenum plays an important role in the process of incorporating fluoride into tooth enamel, as well as in stimulating hematopoiesis.
Molybdenum is part of several enzymes (aldehyde oxidase, sulfite oxidase, xanthine oxidase, etc.) that perform important physiological functions, particularly regulating uric acid metabolism.
Molybdenum enzymes catalyze the hydroxylation of various substrates. For example, aldehyde oxidase oxidizes and neutralizes various pyrimidines, purines, and pteridines. Xanthine oxidase catalyzes the conversion of hypoxanthine to xanthines, and xanthines to uric acid (with increased xanthine oxidase activity in the blood, excessive uric acid accumulates, leading to gout). Sulfite oxidase catalyzes the conversion of sulfite to sulfate.
Molybdenum deficiency in the body is accompanied by a decrease in xanthine oxidase content in tissues. In molybdenum deficiency, anabolic processes are impaired, and there is a weakening of the immune system. Ammonium thiomolybdate (a soluble molybdenum salt) acts as a copper antagonist and disrupts its utilization in the body. There is evidence that molybdenum plays an important role in the process of incorporating fluoride into tooth enamel, as well as in stimulating hematopoiesis.
Synergists and antagonists of molybdenum. It is believed that tungsten, lead, and sodium act as antagonists of molybdenum and cause its deficiency in the body.
Copper sulfate enhances the excretion of molybdenum with bile.
Ammonium thiomolybdate is a copper antagonist and disrupts its utilization in the body.
Deficiency of copper and iron contributes to an increase in molybdenum content in the body.
Copper sulfate enhances the excretion of molybdenum with bile.
Ammonium thiomolybdate is a copper antagonist and disrupts its utilization in the body.
Deficiency of copper and iron contributes to an increase in molybdenum content in the body.
Signs of molybdenum deficiency: increased excitability, irritability, impaired visual (“dark”) adaptation, “night blindness,” disruption of heart rhythm (tachycardia), increased risk of esophageal cancer, decreased activity of molybdenum-containing enzymes.
In cases of molybdenum deficiency (or excess tungsten), the ability to oxidize xanthine to uric acid is impaired, methionine catabolism is inhibited, uric acid and inorganic sulfate excretion is reduced, growth rate decreases, and xanthine stones form in the kidneys. Molybdenum deficiency can lead to reduced cellulose breakdown and excessive copper accumulation in the body, leading to copper toxicity. All these phenomena can be eliminated by adding molybdenum to the diet.
Molybdenum deficiency is possible in individuals receiving total parenteral nutrition or under stress (increased demand for sulfite oxidase). In patients receiving prolonged total parenteral nutrition, a syndrome of “acquired molybdenum deficiency” has been described: hypermethioninemia, hypouricemia, hyperoxypurinemia, hypouricosuria, and hyposulfaturia, with progressive mental disorders (up to coma).
The recognition of the role of molybdenum as a component of sulfite oxidase and data indicating that sulfite oxidase deficiency disrupts cysteine metabolism have been confirmed by cases of disorders caused by the deficiency of functional molybdenum in humans. For instance, there is a congenital defect in cysteine metabolism (sulfite oxidase deficiency) – an anomaly characterized by severe brain damage, mental retardation, lens dislocation, increased urinary excretion of sulfite, decreased urinary excretion of sulfate, which ultimately leads to coma and death. It has been established that in the bodies of patients with congenital cysteine metabolism deficiency, molybdenum is almost absent.
In some regions of the world, endemic diseases are observed related to the degree of molybdenum sufficiency in the population (for example, an increase in esophageal cancer incidence has been noted in Henan Province, China; Transkei, South Africa).
In cases of molybdenum deficiency (or excess tungsten), the ability to oxidize xanthine to uric acid is impaired, methionine catabolism is inhibited, uric acid and inorganic sulfate excretion is reduced, growth rate decreases, and xanthine stones form in the kidneys. Molybdenum deficiency can lead to reduced cellulose breakdown and excessive copper accumulation in the body, leading to copper toxicity. All these phenomena can be eliminated by adding molybdenum to the diet.
Molybdenum deficiency is possible in individuals receiving total parenteral nutrition or under stress (increased demand for sulfite oxidase). In patients receiving prolonged total parenteral nutrition, a syndrome of “acquired molybdenum deficiency” has been described: hypermethioninemia, hypouricemia, hyperoxypurinemia, hypouricosuria, and hyposulfaturia, with progressive mental disorders (up to coma).
The recognition of the role of molybdenum as a component of sulfite oxidase and data indicating that sulfite oxidase deficiency disrupts cysteine metabolism have been confirmed by cases of disorders caused by the deficiency of functional molybdenum in humans. For instance, there is a congenital defect in cysteine metabolism (sulfite oxidase deficiency) – an anomaly characterized by severe brain damage, mental retardation, lens dislocation, increased urinary excretion of sulfite, decreased urinary excretion of sulfate, which ultimately leads to coma and death. It has been established that in the bodies of patients with congenital cysteine metabolism deficiency, molybdenum is almost absent.
In some regions of the world, endemic diseases are observed related to the degree of molybdenum sufficiency in the population (for example, an increase in esophageal cancer incidence has been noted in Henan Province, China; Transkei, South Africa).
With excessive molybdenum consumption – within 10–15 mg/day – clinical symptoms of intoxication appear. At doses of molybdenum exceeding 15 mg/day, xanthine oxidase activity increases, uric acid accumulates, and the risk of gout increases (for example, in individuals exposed to molybdenum in industrial conditions). In chronic molybdenum intoxication, nonspecific symptoms develop, manifesting as irritation of mucous membranes, pneumoconiosis, and weight loss.
With excessive molybdenum content in the soil, an endemic disease is observed – “molybdenum” gout, first observed in the Ankavan region of Armenia by Prof. V.V. Koval’skiy.
With excessive molybdenum content in the soil, an endemic disease is observed – “molybdenum” gout, first observed in the Ankavan region of Armenia by Prof. V.V. Koval’skiy.
Main manifestations of molybdenum excess: increased xanthine oxidase activity, increased uric acid levels in urine; gout (urate excretion and urolithiasis are also possible); irritation of mucous membranes, pneumoconiosis; suppression of hematopoiesis (anemia, leukopenia), weight loss.
Molybdenum is necessary: in brain tumors, vision disorders, tachycardia, male infertility.
Dietary sources of molybdenum: milk and dairy products, liver, kidneys; nuts and seeds: peanuts , cashews , sesame , poppy seeds , macadamia , almonds , Brazil nuts , cedar nuts , sunflower seeds , pumpkin seeds , pistachios , hazelnuts ; fruits: avocados , apricots , pineapples , cherries , strawberries , figs , viburnum , kiwis , cornelian cherries , gooseberries , raspberries , tangerines , sea buckthorn , chokeberry , plums , red currants , black currants , feijoa , persimmons , sweet cherries ; dried fruits: raisins , dried figs , dried apricots , prunes ; vegetables: white cabbage , kohlrabi , cauliflower , potatoes , carrots , hot peppers (chili) , radishes , black radishes , turnips , beets , tomatoes , Jerusalem artichokes , horseradish , garlic ; greens: green onions , lettuce , garlic greens , spinach ; all types of legumes: beans , peas , soybeans , haricot (beans) , lentils ; grains: buckwheat , corn , oats , millet , soft wheat , hard wheat , brown unpolished rice , wild rice , rye and other cereal grains, barley; baked goods.
Poor in molybdenum are some fruits, sugar, oils, fats, and fish.