Introduction

Manganese is a mineral element that is both nutritionally essential and potentially toxic. Scientists are still working to understand the diverse effects of manganese deficiency and manganese toxicity in living organisms. Manganese plays an important role in a number of physiologic processes as a constituent of some enzymes and an activator of other enzymes.

Food Sources

Minerals from plant sources may vary from place to place because soil mineral content varies geographically.

Rich sources of manganese include whole grains, nuts, leafy vegetables, and teas. Foods high in phytic acid such as beans, seeds, nuts, whole grains, and soy products or foods high in oxalic acid such as cabbage, spinach, and sweet potatoes, may slightly inhibit manganese absorption. Although teas are rich sources of manganese, the tannins present in tea may moderately reduce the absorption of manganese.

Some important food sources of Manganese:

Macadamia nuts	Hazelnuts	Peca nuts	Coconutpowder	Almonds
Cashew nuts	Soy beans	Brown rice	Chickpeas	Tea

Recommended Dietary Allowance (RDA)

Since manganese deficiency has not been documented in humans eating natural diets, the European Union has not set an RDA for the general population.

Inhibitors/stimulators:

The following food components have been found to stimulate the absorption of magnesium.

Calcium – Some evidence exists that calcium lowers manganese bioavailability in healthy adults.

Iron – Some evidence suggest that iron and manganese can share common absorption and transport pathways.  Absorption of manganese from a meal is reduced as the meal's iron content is increased.

Magnesium – Supplemental magnesium (200 mg/day) decreased manganese bioavailability slightly, either by decreasing manganese absorption or by increasing its loss in healthy adults.

Functions in the Body

Antioxidant function

Manganese superoxide dismutase (MnSOD) is the principal antioxidant enzyme of mitochondria. Because mitochondria consume over 90% of the oxygen used by cells, they are especially vulnerable to oxidative stress. The superoxide radical is one of the reactive oxygen species produced in mitochondria during ATP synthesis. MnSOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which can be reduced to water by other antioxidant enzymes.

Metabolism

A number of manganese-activated enzymes play important roles in the metabolism of carbohydrates, amino acids, and cholesterol. Pyruvate carboxylase, a manganese-containing enzyme, and phosphoenolpyruvate carboxykinase (PEPCK), a manganese-activated enzyme, play critical roles in gluconeognesis — the production of glucose from non-carbohydrate precursors.  Arginase, another manganese-containing enzyme, is required by the liver for the urea cycle, a process that detoxifies ammonia generated during amino acid metabolism.

Bone development

Manganese deficiency results in abnormal skeletal development in a number of animal species. Manganese is the preferred cofactor of enzymes called glycosyltransferases, which are required for the synthesis of proteoglycans that are needed for the formation of healthy cartilage and bone.

Wound healing

Wound healing is a complex process that requires increased production of collagen. Manganese is required for the activation of prolidase, an enzyme that functions to provide the amino acid proline, essential for collagen formation in human skin cells. A genetic disorder known as prolidase deficiency results in abnormal wound healing (among other problems) and is characterized by abnormal manganese metabolism. Glycosaminoglycan synthesis, which requires manganese-activated glycosyltranserases, may also play an important role in wound healing.

Deficiency

Manganese deficiency has been observed in a number of animal species. In animal species, signs of manganese deficiency include impaired growth, impaired reproductive function, skeletal abnormalities, impaired glucose intolerance, and altered carbohydrate and lipid metabolism. In humans, demonstration of a manganese deficiency syndrome has been less clear. A child on long-term total parenteral nutrition (TPN) that lacked manganese developed bone demineralization and impaired growth that were corrected by manganese supplementation. Young men who were fed a low-manganese diet developed decreased serum cholesterol levels and a transient skin rash. Blood calcium, phosphorus, and alkaline phosphatase levels were also elevated, which may indicate increased bone remodelling as a consequence of insufficient dietary manganese. Young women fed a manganese-poor diet developed mildly abnormal glucose tolerance in response to an intravenous (IV) infusion of glucose.

Toxicity

Manganese toxicity is very unlikely to arise from food, but may arise from inhalation, and ingestion. Inhaled manganese toxicity may result in multiple neurologic problems and is a well-recognized health hazard for people who inhale manganese dust. Unlike ingested manganese, inhaled manganese is transported directly to the brain before it can be metabolized in the liver. The symptoms of manganese toxicity generally appear slowly over a period of months to years. In its worst form, manganese toxicity can result in a permanent neurological disorder with symptoms similar to those of Parkinson's disease, including tremors, difficulty walking, and facial muscle spasms. This syndrome is sometimes preceded by psychiatric symptoms, such as irritability, aggressiveness, and even hallucinations.

High doses of ingested manganese may also result in similar symptoms although there is limited evidence of cases of ingested manganese.

Regulation

Manganese is absorbed with about 4% efficiency from the intestines and is carried into, and in the blood by the protein transmanganin. Regulation of body manganese levels is controlled primarily through variable excretion, rather than absorption.