Manganese is widely distributed in the biosphere: it constitutes approximately 0.085% of the Earth’s crust, making it the twelfth most abundant element. Manganese is a component of numerous complex minerals, including pyroluosite, rhodochrosite, rhodanite, braunite, pyrochite, and manganite. Chemical forms of manganese in their natural depos-its include oxides, sulfides, carbonates, and silicates. Anthropogenic sources of manganese are predomi-nantly from the manufacturing of steel, alloys, and iron products. Manganese is also widely used as an oxidizing agent, as a component of fertilizers and fun-gicides, and in dry cell batteries. The permanganate is a powerful oxidizing agent and is used in quantitative analysis and medicine.
Manganese is a transition element. It can exist in 11 oxidation states from −3 to +7, with the most common valences being +2, +4, and +7. The +2 valence is the predominant form in biological systems, the +4 valence occurs in MnO2, and the +7 valence is found in permanganate.
The total amount of manganese in the adult human is approximately 15 mg. Up to 25% of the total body stores of manganese may be located in the skeleton and may not be readily accessible for use in metabolic pathways. Relatively high concentrations have been reported in the liver, pancreas, intestine, and bone.
Intestinal absorption of manganese occurs through-out the length of the small intestine. Mucosal uptake appears to be mediated by two types of mucosal binding, one that is saturable with a finite capacity and one that is nonsaturable. Manganese absorption, probably as Mn2+, is relatively inefficient, generally less than 5%, but there is some evidence of improve-ment at low intakes. High levels of dietary calcium, phosphorus, and phytate impair the intestinal uptake of the element but are probably of limited significance because, as yet, no well-documented case of human manganese deficiency has been reported.
Systemic homeostatic regulation of manganese is brought about primarily through hepatobiliary excretion rather than through regulation of absorp-tion (e.g., the efficiency of manganese retention does not appear to be dose dependent within normal dietary levels). Manganese is taken up from blood by the liver and transported to extrahepatic tissues by transferrin and possibly α2-macroglobulin and albumin. Manga-nese is excreted primarily in feces. Urinary excretion of manganese is low and has not been found to be sensi-tive to dietary manganese intake.
Manganese is required as a catalytic cofactor for mitochondrial superoxide dismutase, arginase, and pyruvate carboxylase. It is also an activator of glycos-yltransferases, phosphoenolpyruvate carboxylase, and glutamine synthetase.
Signs of manganese deficiency have been demon-strated in several animal species. Symptoms include impaired growth, skeletal abnormalities, depressed reproductive function, and defects in lipid and carbo-hydrate metabolism. Evidence of manganese defi-ciency in humans is poor. It has been suggested that manganese deficiency has never been observed in noninstitutionalized human populations because of the abundant supply of manganese in edible plant materials compared with the relatively low require-ments of mammals. There is only one report of apparent human manganese deficiency. A male subject was fed a purified diet deficient in vitamin K, which was accidentally also deficient in manganese. Feeding this diet caused weight loss, dermatitis, growth retar-dation of hair and nails, reddening of black hair, and a decline in concentrations of blood lipids. Manganese deficiency may be more frequent in infants owing to the low concentration of manganese in human breast milk and varying levels in infant formulae.
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