by a different mechanism. The molecular characteristics of the magnesium transport proteins have not been described.

Magnesium transport in mammalian cells may be influenced by hormonal and pharmacological factors including β-agonists, growth factors, and insulin (Gunther, 1993; Hwang et al., 1993; Romani et al., 1993). It has been suggested that a hormonally regulated magnesium uptake system controls intracellular magnesium concentration in cellular compartments. The magnesium concentration in these compartments would then serve to regulate the activity of magnesium-sensitive enzymes.

Magnesium presence is important for maintaining an adequate supply of purine and pyrimidine nucleotides required for the increased DNA and RNA synthesis that occurs during cell proliferation (Rubin, 1975; Switzer, 1971). Replicating cells must be able to synthesize new protein, and this synthesis has been reported to be highly sensitive to magnesium depletion. Many hormones, neurotransmitters, and other cellular effectors regulate cellular activity via the adenylate cyclase system, and the activation of adenylate cyclase requires the presence of magnesium. There is also evidence for magnesium binding through which magnesium directly increases adenylate cyclase activity (Maguire, 1984).

Magnesium is necessary for sodium, potassium-ATPase activity, which is responsible for active transport of potassium (Dorup and Clausen, 1993). Magnesium regulates the outward movement of potassium in myocardial cells (Matsuda, 1991). The arrhythmogenic effect of magnesium deficiency may be related to magnesium's role in maintaining intracellular potassium.

Magnesium has been called “nature's physiological calcium channel blocker” (Iseri and French, 1984). During magnesium depletion, intracellular calcium rises. Since calcium plays an important role in skeletal and smooth muscle contraction, a state of magnesium depletion may result in muscle cramps, hypertension, and coronary and cerebral vasospasms. Magnesium depletion is found in a number of diseases of cardiovascular and neuromuscular function, in malabsorption syndromes, in diabetes mellitus, in renal wasting syndromes, and in alcoholism (Ma et al., 1995). These observations have led to studies regarding the role of inadequate magnesium intake in the development of disease, as opposed to abnormal handling of magnesium caused by the disease process. It is important to ensure that such evaluations are undertaken in apparently normal individuals for whom dietary intake is the primary independent variable.

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