Manganese is a trace element. It occurs widely in plant and animal tissues
and is an essential element for many animal species. Manganese absorption occurs
throughout the small intestine. The exact mechanism of absorption is unknown,
although it is thought to occur by a two-step mechanism that involves an initial
uptake from the lumen followed by active transport across the mucosal cells. A
specific manganese-carrying plasma protein called transmanganin has been
identified. Almost all absorbed manganese is excreted with the feces; only trace
amounts are found in the urine. Absorption efficiency is estimated to be roughly
5% and may decline as dietary intake increases. The retention of manganese is
estimated to be 10%, 14 days after feeding. The human body contains a mere 20 mg
of manganese, mostly in cell mitochondria. Organs rich in mitochondria, such as
liver, kidney, and pancreas have relatively high manganese concentrations. Bone
has the highest concentration of manganese.
Manganese serves two primary biochemical functions in the body, (1) it
activates specific enzymes, and (2) it is a constituent of several
metalloenzymes. The enzymes manganese activates include hydrolases,
decarboxylases, kinases, and transferases. Certain other ions (cobalt,
magnesium) can replace its function in this capacity. The manganese
metalloenzymes include arginase, pyruvate carboxylase, glutamine synthetase, and
manganese superoxide dismutase.
Manganese participates in numerous biochemical functions in the body
including steroid and sulfomucopolysacchride biosynthesis, carbohydrate and
lipid metabolism, and bone, blood clot, and protein formation. It is also
essential for normal brain function, possibly through its role in biogenic amine
metabolism. Many of the precise biochemical roles of manganese have not been
Manganese deficiency has been induced in several animal species, but not in
humans. Deficiency symptoms in animals include skeletal abnormalities, impaired
growth, disturbed or depressed reproductive function, ataxia of the newborn, and
defects in lipid and carbohydrate metabolism. Although frank deficiency symptoms
have not been observed in humans, biochemical evidence has established its
essentiality in humans. Impaired fertility, growth retardation, birth defects,
bone malformations, seizures, and general weakness may result from manganese
- Nuts (especially pecans, almonds)
- Wheat germ and whole grains
- Unrefined cereals
- Leafy vegetables
- Dried fruits
Refined grains, meats, and dairy products contain only small amounts of
manganese. Highly refined diets contain significantly less manganese (0.36 to
1.78 mg) than diets high in unrefined foods (8.3 mg).
Mn2+ is the characteristic oxidative state of manganese in
solution, in metal enzyme complexes, and in metalloenzymes. Mn3+ is
the oxidative state in the enzyme manganese superoxide dismutase (MnSOD), and
the form that binds to transferrin and interacts with
Manganese is available commercially in a wide variety of forms including
manganese salts (sulfate and chloride) and manganese chelates (gluconate,
picolinate, aspartate, fumarate, malate, succinate, citrate, and amino acid
chelate). Preparation doses are typically between 2 and 20
- Diabetes: Type I and II diabetics have significantly less manganese
than healthy individuals. Diabetics with liver disorders and those not on
insulin therapy may excrete more manganese. Manganese appears to have a
hypoglycemic effect and may decrease blood glucose levels in insulin-resistant
- Rheumatoid arthritis: RA, as well as other inflammation brought on by
strains and sprains may respond well to manganese treatment. Levels of MnSOD may
be significantly decreased in individuals with rheumatoid arthritis. Manganese
supplementation increases MnSOD activity.
- Epilepsy: An important study in the early 1960s demonstrated that
manganese-deficient rats were more susceptible to seizures, and had EEG tracings
consistent with seizure activity. People who have schizophrenia may also respond
well to magnesium supplementation.
- Osteoporosis: Manganese, and other trace elements, increase spinal
bone mineral density in postmenopausal women.
- Immunocompetence and cancer: Adequate manganese is necessary for
normal antibody production. Excessive or inadequate manganese intakes may affect
neutrophil and macrophage function.
- Cadmium toxicity: Manganese reduces toxic effects of cadmium in
- Other conditions: Manganese is also used to treat atherosclerosis,
hypercholesterolemia, tinnitus, and hearing loss.
- Total parenteral nutrition (TPN): Bone changes may occur in patients
given TPN solutions containing inadequate quantities of manganese. In contrast,
cholestatic and nervous system disorders have been associated with high blood
concentrations of manganese from long-term TPN treatment. Children's TPN
solutions should contain low-dose manganese (0.018 mucmol/kg per 24 hours).
|Dosage Ranges and Duration of
The exact amount of manganese required by the human body is not known. The
Food and Nutrition Board (FNB) of the National Research Council (NRC) has
established estimated safe and adequate daily intakes for manganese as
- Infants 0 to 0.5 years: 0.3 to 0.6 mg
- Infants 0.5 to 1 year: 0.6 to 1.0 mg
- Children 1 to 3 years: 1.0 to 1.5 mg
- Children 4 to 6 years: 1.5 to 2.0 mg
- Children 7 to 10 years: 2.0 to 3.0 mg
- Adolescents 11+ years: 2.0 to 5.0 mg
- Adults: 2.0 to 5.0 mg.
These estimates are based on the assumption that most dietary intakes fall in
this range and do not result in deficiency or toxicity signs. The estimates may
be modified as additional information becomes available. More manganese (10
mg/day) should be consumed if the diet contains high amounts of substances that
inhibit manganese absorption. In therapeutic use for epilepsy, inflammation, or
diarrhea, the dose may be increased three-to-sixfold.
Manganese is one of the least toxic of the trace elements, though excessive
intake may produce toxic effects. There are only a few reports of oral manganese
poisoning in man. Manganese toxicity is more common in humans chronically
exposed to manganese dust found in steel mills and mines and certain chemical
industries. Toxicity principally affects the brain, causing severe psychiatric
abnormalities, but may also increase blood pressure in the doses used to treat
The FNB of the NRC recommends that the upper limits for the trace elements
should not be habitually exceeded because the toxicity levels may be only
several times usual intakes.
In one case report, a patient with progressive hepatic failure who received
haloperidol and manganese as part of total parenteral nutrition exhibited
neuropsychiatric symptoms (Mehta and Reilly 1990). Toxic manganese levels may
have increased the patient's susceptiblity to haloperidol toxicity.
Simultaneous administration of phenobarbital and manganese (5 mg/kg)
prevented manganese-induced prolongation of hexobarbital hypnosis in male rats
(Deimling and Schnell 1983).
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